HapMap imputed genome-wide association studies (GWAS) have revealed >50 loci at which common variants with minor allele frequency >5% are associated with kidney function. GWAS using more complete reference sets for imputation, such as those from The 1000 Genomes project, promise to identify novel loci that have been missed by previous efforts. To investigate the value of such a more complete variant catalog, we conducted a GWAS meta-analysis of kidney function based on the estimated glomerular filtration rate (eGFR) in 110,517 European ancestry participants using 1000 Genomes imputed data. We identified 10 novel loci with p-value < 5 × 10−8 previously missed by HapMap-based GWAS. Six of these loci (HOXD8, ARL15, PIK3R1, EYA4, ASTN2, and EPB41L3) are tagged by common SNPs unique to the 1000 Genomes reference panel. Using pathway analysis, we identified 39 significant (FDR < 0.05) genes and 127 significantly (FDR < 0.05) enriched gene sets, which were missed by our previous analyses. Among those, the 10 identified novel genes are part of pathways of kidney development, carbohydrate metabolism, cardiac septum development and glucose metabolism. These results highlight the utility of re-imputing from denser reference panels, until whole-genome sequencing becomes feasible in large samples. ; 3C. Three-City Study. The work was made possible by the participation of the control subjects, the patients, and their families. We thank Dr. Anne Boland (CNG) for her technical help in preparing the DNA samples for analyses. This work was supported by the National Foundation for Alzheimer's disease and related disorders, the Institut Pasteur de Lille and the Centre National de Génotypage. The 3C Study was performed as part of a collaboration between the Institut National de la Santé et de la Recherche Médicale (Inserm), the Victor Segalen Bordeaux II University and Sanofi-Synthélabo. The Fondation pour la Recherche Médicale funded the preparation and initiation of the study. The 3C Study was also funded by the Caisse Nationale Maladie des Travailleurs Salariés, Direction Générale de la Santé, MGEN, Institut de la Longévité, Agence Française de Sécurité Sanitaire des Produits de Santé, the Aquitaine and Bourgogne Regional Councils, Fondation de France and the joint French Ministry of Research/INSERM "Cohortes et collections de données biologiques" programme. Lille Génopôle received an unconditional grant from Eisai. AGES. Age, Gene/Environment Susceptibility-Reykjavik Study. This study has been funded by NIH contract N01-AG-1-2100, the NIA Intramural Research Program, Hjartavernd (the Icelandic Heart Association), and the Althingi (the Icelandic Parliament). The study is approved by the Icelandic National Bioethics Committee, VSN: 00-063. The researchers are indebted to the participants for their willingness to participate in the study. ARIC. Atherosclerosis Risk in Communities study. The ARIC study is carried out as a collaborative study supported by National Heart, Lung, and Blood Institute contracts (HHSN268201100005C, HHSN268201100006C, HHSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C), R01HL087641, R01HL59367 and R01HL086694; National Human Genome Research Institute contract U01HG004402; and National Institutes of Health contract HHSN268200625226C. The authors thank the staff and participants of the ARIC study for their important contributions. Infrastructure was partly supported by Grant Number UL1RR025005, a component of the National Institutes of Health and NIH Roadmap for Medical Research. This work as well as YL and AK were supported by the German Research Foundation (KO 3598/2-1, KO 3598/3-1 and CRC1140 A05 to AK). ASPS. Austrian Stroke Prevention Study. The research reported in this article was funded by the Austrian Science Fond (FWF) grant number P20545-P05 and P13180. The Medical University of Graz supports the databank of the ASPS. The authors thank the staff and the participants of the ASPS for their valuable contributions. We thank Birgit Reinhart for her long-term administrative commitment and Ing Johann Semmler for the technical assistance at creating the DNA-bank. BMES. Blue Mountains Eye Study. The BMES has been supported by the Australian RADGAC grant (1992- 94) and Australian National Health & Medical Research Council, Canberra Australia (Grant Nos: 974159, 211069, 991407, 457349). The GWAS studies of Blue Mountains Eye Study population are supported by the Australian National Health & Medical Research Council (Grant Nos: 512423, 475604, 529912) and the Wellcome Trust, UK (2008). EGH and JJW are funded by the Australian National Health & Medical Research Council Fellowship Schemes. CILENTO. Italian Network on Genetic Isolates – Cilento. We thank the populations of Cilento for their participation in the study. The study was supported by the Italian Ministry of Universities and CNR 36 (PON03PE_00060_7, Interomics Flagship Project), the Assessorato Ricerca Regione Campania, the Fondazione con il SUD (2011-PDR-13), and the Istituto Banco di Napoli - Fondazione to MC. COLAUS. The CoLaus authors thank Yolande Barreau, Mathieu Firmann, Vladimir Mayor, Anne-Lise Bastian, Binasa Ramic, Martine Moranville, Martine Baumer, Marcy Sagette, Jeanne Ecoffey and Sylvie Mermoud for data collection. The CoLaus study received financial contributions from GlaxoSmithKline, the Faculty of Biology and Medicine of Lausanne, the Swiss National Science Foundation (33CSCO- 122661, 3200BO-111361/2, 3100AO-116323/1, 310000-112552). The computations for CoLaus imputation were performed in part at the Vital-IT center for high performance computing of the Swiss Institute of Bioinformatics. We thank Vincent Mooser for his contribution to the CoLaus study. EGCUT. Estonian Genome Center University of Tartu. EGCUT received financing from FP7 grants (278913, 306031, 313010) and targeted financing from Estonian Government (SF0180142s08). EGCUT studies were covered from Infra-structure grant no. 3.2.0304.11-0312 funded mostly by the European Regional Development Fund, Center of Excellence in Genomics (EXCEGEN) and University of Tartu (SP1GVARENG). We acknowledge EGCUT technical personnel, especially Mr V. Soo and S. Smit. Data analyses were carried out in part in the High Performance Computing Center of the University of Tartu. FamHS. Family Heart Study. The FHS work was supported in part by NIH grants 5R01HL08770003, 5R01HL08821502 (Michael A. Province) from the NHLBI and 5R01DK07568102, 5R01DK06833603 from the NIDDK (I.B.B.). The authors thank the staff and participants of the FamHS for their important contributions. FHS. Framingham Heart Study. This research was conducted in part using data and resources from the Framingham Heart Study of the National Heart Lung and Blood Institute of the National Institutes of Health and Boston University School of Medicine. The analyses reflect intellectual input and resource development from the Framingham Heart Study investigators participating in the SNP Health Association Resource (SHARe) project. This work was partially supported by the National Heart, Lung and Blood Institute's Framingham Heart Study (Contract No. N01-HC-25195) and its contract with Affymetrix, Inc. for genotyping services (Contract No. N02-HL-6-4278). A portion of this research utilized the Linux Cluster for Genetic Analysis (LinGA-II) funded by the Robert Dawson Evans Endowment of the Department of Medicine at Boston University School of Medicine and Boston Medical Center. GENDIAN. GENetics of DIAbetic Nephropathy study. The support of the physicians, the patients, and the staff of the Diabetes Zentrum Mergentheim (Head: Prof. Dr. Thomas Haak), the diabetes outpatient clinic Dr Nusser - Dr Kreisel, the dialysis centers KfH Amberg, KfH Bayreuth, KfH Deggendorf, KfH Donauwörth, KfH Freising, KfH Freyung, KfH Fürth, KfH Hof, KfH Ingolstadt, KfH Kelheim, KfH München Elsenheimerstraße, KfH München-Schwabing, KfH Neumarkt, KfH Neusäß, KfH Oberschleißheim, KfH Passau, KfH Plauen, KfH Regensburg Günzstraße, KfH Regensburg Caritas-Krankenhaus, KfH Straubing, KfH Sulzbach-Rosenberg, KfH Weiden, Dialysezentrum Augsburg Dr. Kirschner, Dialysezentrum Bad Alexandersbad, KfH Bamberg, Dialysezentrum Emmering, Dialysezentrum Klinikum Landshut, Dialysezentrum Landshut, Dialysezentrum Pfarrkirchen, Dialysezentrum Schwandorf, Dr. Angela Götz, the medical doctoral student Johanna Christ and the Study Nurse Ingrid Lugauer. The expert technical assistance of Claudia Strohmeier is acknowledged. Phenotyping was funded by the Dr. Robert PflegerStiftung (Dr Carsten A. Böger), the MSD Stipend Diabetes (Dr Carsten A. Böger) and the University Hospital of Regensburg (intramural grant ReForM A to Dr. A. Götz, ReForM C to Dr. Carsten Böger). Genome-wide genotyping was funded by the KfH Stiftung Präventivmedizin e.V. (Dr. Carsten A. Böger, Dr. Jens Brüning), the Else Kröner-Fresenius-Stiftung (2012_A147 to Dr Carsten A. Böger and Dr Iris M. Heid) and the University Hospital Regensburg (Dr Carsten A. Böger). Data analysis was funded by the Else 37 Kröner-Fresenius Stiftung (Dr. Iris M. Heid and Dr. Carsten A. Böger: 2012_A147; Dr. Carsten A. Böger and Dr. Bernhard K. Krämer: P48/08//A11/08). GENDIAN Study Group: Mathias Gorski, Iris M. Heid, Bernhard K. Krämer, Myriam Rheinberger, Michael Broll, Alexander Lammert, Jens Brüning, Matthias Olden, Klaus Stark, Claudia Strohmeier, Simone Neumeier, Sarah Hufnagel, Petra Jackermeier, Emilia Ruff, Johanna Christ, Peter Nürnberg, Thomas Haak, Carsten A. Böger. HABC. Health Aging and Body Composition Study. The HABC study was funded by the National Institutes of Aging. This research was supported by NIA contracts N01AG62101, N01AG62103, and N01AG62106. The genome-wide association study was funded by NIA grant 1R01AG032098-01A1 to Wake Forest University Health Sciences and genotyping services were provided by the Center for Inherited Disease Research (CIDR). CIDR is fully funded through a federal contract from the National Institutes of Health to The Johns Hopkins University, contract number HHSN268200782096C. This research was supported in part by the Intramural Research Program of the NIH, National Institute on Aging. HCS. Hunter Community Study. The University of Newcastle provided $300,000 from its Strategic Initiatives Fund, and $600,000 from the Gladys M Brawn Senior Research Fellowship scheme; Vincent Fairfax Family Foundation, a private philanthropic trust, provided $195,000; The Hunter Medical Research Institute provided media support during the initial recruitment of participants; and Dr Anne Crotty, Prof. Rodney Scott and Associate Prof. Levi provided financial support towards freezing costs for the long-term storage of participant blood samples. The authors would like to thank the men and women participating in the HCS as well as all the staff, investigators and collaborators who have supported or been involved in the project to date. A special thank you should go to Alison Koschel and Debbie Quain who were instrumental in setting up the pilot study and initial phase of the project. HPFS. Health Professionals Follow-Up Study. The NHS/HPFS type 2 diabetes GWAS (U01HG004399) is a component of a collaborative project that includes 13 other GWAS (U01HG004738, U01HG004422, U01HG004402, U01HG004729, U01HG004726, U01HG004735, U01HG004415, U01HG004436, U01HG004423, U01HG004728, RFAHG006033; National Institute of Dental & Craniofacial Research: U01DE018993, U01DE018903) funded as part of the Gene Environment-Association Studies (GENEVA) under the NIH Genes, Environment and Health Initiative (GEI). Assistance with phenotype harmonization and genotype cleaning, as well as with general study coordination, was provided by the GENEVA Coordinating Center (U01HG004446). Assistance with data cleaning was provided by the National Center for Biotechnology Information. Genotyping was performed at the Broad Institute of MIT and Harvard, with funding support from the NIH GEI (U01HG04424), and Johns Hopkins University Center for Inherited Disease Research, with support from the NIH GEI (U01HG004438) and the NIH contract "High throughput genotyping for studying the genetic contributions to human disease"(HHSN268200782096C). Additional funding for the current research was provided by the National Cancer Institute (P01CA087969, P01CA055075), and the National Institute of Diabetes and Digestive and Kidney Diseases (R01DK058845). We thank the staff and participants of the NHS and HPFS for their dedication and commitment. INGI-CARLANTINO. Italian Network on Genetic Isolates – Carlantino. We thank Anna Morgan and Angela D'Eustacchio for technical support. We are grateful to the municipal administrators for their collaboration on the project and for logistic support. We thank all participants to this study. INGI-FVG. Italian Network on Genetic Isolates – Friuli Venezia-Giulia. We thank Anna Morgan and Angela D'Eustacchio for technical support. We are grateful to the municipal administrators for their collaboration on the project and for logistic support. We thank all participants to this study. 38 INGI-VAL BORBERA. Italian Network on Genetic Isolates – Val Borbera. We thank the inhabitants of the Val Borbera who made this study possible, the local administrations and the ASL-Novi Ligure (Al) for support. We also thank Clara Camaschella for data collection supervision and organization of the clinical data collection, Fiammetta Vigano` for technical help and Corrado Masciullo for building the analysis platform. The research was supported by funds from Compagnia di San Paolo, Torino, Italy; Fondazione Cariplo, Italy and Ministry of Health, Ricerca Finalizzata 2008 and 2011/2012, CCM 2010, PRIN 2009 and Telethon, Italy to DT. IPM. Mount Sinai BioMe Biobank Program. The Mount Sinai BioMe Biobank Program is supported by The Andrea and Charles Bronfman Philanthropies. KORA-F3 and F4. The genetic epidemiological work was funded by the NIH subcontract from the Children's Hospital, Boston, US, (H.E.W., I.M.H, prime grant 1 R01 DK075787-01A1), the German National Genome Research Net NGFN2 and NGFNplus (H.E.W. 01GS0823; WK project A3, number 01GS0834), the Munich Center of Health Sciences (MC Health) as part of LMUinnovativ, and by the Else KrönerFresenius-Stiftung (P48/08//A11/08; C.A.B., B.K.K; 2012_A147 to CAB and IMH.). The Genetic Epidemiology at the University of Regensburg received financial contributions from the BMBF (01ER1206 and 01ER1507). The kidney parameter measurements in F3 were funded by the Else Kröner-FreseniusStiftung (C.A.B., B.K.K.) and the Regensburg University Medical Center, Germany; in F4 by the University of Ulm, Germany (W.K.). Genome wide genotyping costs in F3 and F4 were in part funded by the Else Kröner-Fresenius-Stiftung (C.A.B., B.K.K.). De novo genotyping in F3 and F4 were funded by the Else Kröner-Fresenius-Stiftung (C.A.B., B.K.K.). The KORA research platform and the MONICA Augsburg studies were initiated and financed by the Helmholtz Zentrum München, German Research Center for Environmental Health, by the German Federal Ministry of Education and Research and by the State of Bavaria. Genotyping was performed in the Genome Analysis Center (GAC) of the Helmholtz Zentrum München. The LINUX platform for computation were funded by the University of Regensburg for the Department of Epidemiology and Preventive Medicine at the Regensburg University Medical Center. LIFELINES. The authors wish to acknowledge the services of the Lifelines Cohort Study, the contributing research centers delivering data to Lifelines, and all the study participants. Lifelines group authors: Behrooz Z Alizadeh1 , H Marike Boezen1 , Lude Franke2 , Pim van der Harst3 , Gerjan Navis4 , Marianne Rots5 , Harold Snieder1 , Morris Swertz2 , Bruce HR Wolffenbuttel6 and Cisca Wijmenga2 1. Department of Epidemiology, University of Groningen, University Medical Center Groningen, The Netherlands 2. Department of Genetics, University of Groningen, University Medical Center Groningen, The Netherlands 3. Department of Cardiology, University of Groningen, University Medical Center Groningen, The Netherlands 4. Department of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, The Netherlands 5. Department of Medical Biology, University of Groningen, University Medical Center Groningen, The Netherlands 6. Department of Endocrinology, University of Groningen, University Medical Center Groningen, The Netherlands MESA. Multi-Ethnic Study of Atherosclerosis. University of Washington (N01-HC-95159),Regents of the University of California (N01-HC-95160), Columbia University (N01-HC-95161), Johns Hopkins University 39 (N01-HC-95162, N01-HC-95168), University of Minnesota (N01-HC-95163), Northwestern University (N01-HC-95164), Wake Forest University (N01-HC-95165), University of Vermont (N01-HC-95166), New England Medical Center (N01-HC-95167), Harbor-UCLA Research and Education Institute (N01-HC- 95169), Cedars-Sinai Medical Center (R01-HL-071205), University of Virginia (subcontract to R01-HL- 071205) MICROS. Microisolates in South Tyrol study. We owe a debt of gratitude to all participants. We thank the primary care practitioners R. Stocker, S. Waldner, T. Pizzecco, J. Plangger, U. Marcadent and the personnel of the Hospital of Silandro (Department of Laboratory Medicine) for their participation and collaboration in the research project. In South Tyrol, the study was supported by the Ministry of Health and Department of Educational Assistance, University and Research of the Autonomous Province of Bolzano, the South Tyrolean Sparkasse Foundation, and the European Union framework program 6 EUROSPAN project (contract no. LSHG-CT-2006-018947). NESDA. The Netherlands Study of Depression and Anxiety. The infrastructure for the NESDA study is funded through the Geestkracht programme of the Dutch Scientific Organization (ZON-MW, grant number 10-000-1002) and matching funds from participating universities and mental health care organizations. Genotyping in NESDA was funded by the Genetic Association Information Network (GAIN) of the Foundation for the US National Institutes of Health. NHS. Nurses' Health Study. The NHS/HPFS type 2 diabetes GWAS (U01HG004399) is a component of a collaborative project that includes 13 other GWAS (U01HG004738, U01HG004422, U01HG004402, U01HG004729, U01HG004726, U01HG004735, U01HG004415, U01HG004436, U01HG004423, U01HG004728, RFAHG006033; National Institute of Dental & Craniofacial Research: U01DE018993, U01DE018903) funded as part of the Gene Environment-Association Studies (GENEVA) under the NIH Genes, Environment and Health Initiative (GEI). Assistance with phenotype harmonization and genotype cleaning, as well as with general study coordination, was provided by the GENEVA Coordinating Center (U01HG004446). Assistance with data cleaning was provided by the National Center for Biotechnology Information. Genotyping was performed at the Broad Institute of MIT and Harvard, with funding support from the NIH GEI (U01HG04424), and Johns Hopkins University Center for Inherited Disease Research, with support from the NIH GEI (U01HG004438) and the NIH contract "High throughput genotyping for studying the genetic contributions to human disease"(HHSN268200782096C). The NHS renal function and albuminuria work was supported by DK66574. Additional funding for the current research was provided by the National Cancer Institute (P01CA087969, P01CA055075), and the National Institute of Diabetes and Digestive and Kidney Diseases (R01DK058845). We thank the staff and participants of the NHS and HPFS for their dedication and commitment. NSPHS. The Northern Swedish Population Health Study. The NSPHS was supported by grants from the Swedish Natural Sciences Research Council, the European Union through the EUROSPAN project (contract no. LSHG-CT-2006-018947), the Foundation for Strategic Research (SSF) and the Linneaus Centre for Bioinformatics (LCB). We are also grateful for the contribution of samples from the Medical Biobank in Umeå and for the contribution of the district nurse Svea Hennix in the Karesuando study. RS-I. The Rotterdam Study. The GWA study was funded by the Netherlands Organisation of Scientific Research NWO Investments (nr. 175.010.2005.011, 911-03-012), the Research Institute for Diseases in the Elderly (014-93-015; RIDE2), the Netherlands Genomics Initiative (NGI)/Netherlands Consortium for Healthy Aging (NCHA) project nr. 050-060-810. We thank Pascal Arp, Mila Jhamai, Dr Michael 40 Moorhouse, Marijn Verkerk, and Sander Bervoets for their help in creating the GWAS database. The Rotterdam Study is funded by Erasmus Medical Center and Erasmus University, Rotterdam, Netherlands Organization for the Health Research and Development (ZonMw), the Research Institute for Diseases in the Elderly (RIDE), the Ministry of Education, Culture and Science, the Ministry for Health, Welfare and Sports, the European Commission (DG XII), and the Municipality of Rotterdam. The authors are very grateful to the participants and staff from the Rotterdam Study, the participating general practitioners and the pharmacists. We would like to thank Dr. Tobias A. Knoch, Luc V. de Zeeuw, Anis Abuseiris, and Rob de Graaf as well as their institutions the Erasmus Computing Grid, Rotterdam, The Netherlands, and especially the national German MediGRID and Services@MediGRID part of the German D-Grid, both funded by the German Bundesministerium fuer Forschung und Technology under grants #01 AK 803 A-H and # 01 IG 07015 G, for access to their grid resources. Abbas Dehghan is supported by NWO grant (vici, 918-76-619). SAPALDIA. Swiss Study on Air Pollution and Lung Diseases in Adults. The SAPALDIA Team: Study directorate: T Rochat (p), NM Probst Hensch (e/g), N Künzli (e/exp), C Schindler (s), JM Gaspoz (c) Scientific team: JC Barthélémy (c), W Berger (g), R Bettschart (p), A Bircher (a), O Brändli (p), C Brombach (n), M Brutsche (p), L Burdet (p), M Frey (p), U Frey (pd), MW Gerbase (p), D Gold (e/c/p), E de Groot (c), W Karrer (p), R Keller (p), B Martin (pa), D Miedinger (o), U Neu (exp), L Nicod (p), M Pons (p), F Roche (c), T Rothe (p), E Russi (p), P Schmid-Grendelmeyer (a), A Schmidt-Trucksäss (pa), A Turk (p), J Schwartz (e), D. Stolz (p), P Straehl (exp), JM Tschopp (p), A von Eckardstein (cc), E Zemp Stutz (e). Scientific team at coordinating centers: M Adam (e/g), C Autenrieth (pa), PO Bridevaux (p), D Carballo (c), E Corradi (exp), I Curjuric (e), J Dratva (e), A Di Pasquale (s), E Dupuis Lozeron (s), E Fischer (e), M Germond (s), L Grize (s), D Keidel (s), S Kriemler (pa), A Kumar (g), M Imboden (g), N Maire (s), A Mehta (e), H Phuleria (exp), E Schaffner (s), GA Thun (g) A Ineichen (exp), M Ragettli (e), M Ritter (exp), T Schikowski (e), M Tarantino (s), M Tsai (exp) (a) allergology, (c) cardiology, (cc) clinical chemistry, (e) epidemiology, (exp) exposure, (g) genetic and molecular biology, (m) meteorology, (n) nutrition, (o) occupational health, (p) pneumology, (pa) physical activity, (pd) pediatrics, (s) statistics. Funding: The Swiss National Science Foundation (grants no 33CSCO-134276/1, 33CSCO-108796, 3247BO-104283, 3247BO-104288, 3247BO- 104284, 3247-065896, 3100-059302, 3200-052720, 3200-042532, 4026-028099), the Federal Office for Forest, Environment and Landscape, the Federal Office of Public Health, the Federal Office of Roads and Transport, the canton's government of Aargau, Basel-Stadt, Basel-Land, Geneva, Luzern, Ticino, Valais, and Zürich, the Swiss Lung League, the canton's Lung League of Basel Stadt/ Basel Landschaft, Geneva, Ticino, Valais and Zurich, SUVA, Freiwillige Akademische Gesellschaft, UBS Wealth Foundation, Talecris Biotherapeutics GmbH, Abbott Diagnostics, European Commission 018996 (GABRIEL), Wellcome Trust WT 084703MA. The study could not have been done without the help of the study participants, technical and administrative support and the medical teams and field workers at the local study sites. Local fieldworkers : Aarau: S Brun, G Giger, M Sperisen, M Stahel, Basel: C Bürli, C Dahler, N Oertli, I Harreh, F Karrer, G Novicic, N Wyttenbacher, Davos: A Saner, P Senn, R Winzeler, Geneva: F Bonfils, B Blicharz, C Landolt, J Rochat, Lugano: S Boccia, E Gehrig, MT Mandia, G Solari, B Viscardi, Montana: AP Bieri, C Darioly, M Maire, Payerne: F Ding, P Danieli A Vonnez, Wald: D Bodmer, E Hochstrasser, R Kunz, C Meier, J Rakic, U Schafroth, A Walder. Administrative staff: C Gabriel, R Gutknecht. SHIP and SHIP-TREND. The Study of Health in Pomerania. SHIP is part of the Community Medicine Research net of the University of Greifswald, Germany, which is funded by the Federal Ministry of Education and Research (grants no. 01ZZ9603, 01ZZ0103, and 01ZZ0403), the Ministry of Cultural Affairs as well as the Social Ministry of the Federal State of Mecklenburg-West Pomerania, and the network 41 'Greifswald Approach to Individualized Medicine (GANI_MED)' funded by the Federal Ministry of Education and Research (grant 03IS2061A). Genome-wide data have been supported by the Federal Ministry of Education and Research (grant no. 03ZIK012) and a joint grant from Siemens Healthcare, Erlangen, Germany and the Federal State of Mecklenburg- West Pomerania. The University of Greifswald is a member of the 'Center of Knowledge Interchange' program of the Siemens AG and the Caché Campus program of the InterSystems GmbH. The SHIP authors are grateful to Mario Stanke for the opportunity to use his Server Cluster for the SNP imputation as well as to Holger Prokisch and Thomas Meitinger (Helmholtz Zentrum München) for the genotyping of the SHIP-TREND cohort. TRAILS. TRacking Adolescents' Individual Lives. Trails is a collaborative project involving various departments of the University Medical Center and University of Groningen, the Erasmus University Medical Center Rotterdam, the University of Utrecht, the Radboud Medical Center Nijmegen, and the Parnassia Bavo group, all in the Netherlands. TRAILS has been financially supported by grants from the Netherlands Organization for Scientific Research NWO (Medical Research Council program grant GB-MW 940-38-011; ZonMW Brainpower grant 100-001-004; ZonMw Risk Behavior and Dependence grants 60- 60600-98-018 and 60-60600-97-118; ZonMw Culture and Health grant 261-98-710; Social Sciences Council medium-sized investment grants GB-MaGW 480-01-006 and GB-MaGW 480-07-001; Social Sciences Council project grants GB-MaGW 457-03-018, GB-MaGW 452-04-314, and GB-MaGW 452-06- 004; NWO large-sized investment grant 175.010.2003.005; NWO Longitudinal Survey and Panel Funding 481-08-013); the Sophia Foundation for Medical Research (projects 301 and 393), the Dutch Ministry of Justice (WODC), the European Science Foundation (EuroSTRESS project FP-006), and the participating universities. We are grateful to all adolescents, their parents and teachers who participated in this research and to everyone who worked on this project and made it possible. Statistical analyses were carried out on the Genetic Cluster Computer (http://www.geneticcluster.org), which is financially supported by the Netherlands Scientific Organization (NWO 480-05-003) along with a supplement from the Dutch Brain Foundation. WGHS. Women's Genome Health Study. The WGHS is supported by the National Heart, Lung, and Blood Institute (HL043851 and HL080467) and the National Cancer Institute (CA047988 and UM1CA182913), with collaborative scientific support and funding for genotyping provided by Amgen. YFS. Young Finns Study. The YFS has been financially supported by the Academy of Finland: grants 134309 (Eye), 126925, 121584, 124282, 129378 (Salve), 117787 (Gendi), and 41071 (Skidi), the Social Insurance Institution of Finland, Kuopio, Tampere and Turku University Hospital Medical Funds (grant 9M048 and 9N035 for TeLeht), Juho Vainio Foundation, Paavo Nurmi Foundation, Finnish Foundation of Cardiovascular Research and Finnish Cultural Foundation, Tampere Tuberculosis Foundation and Emil Aaltonen Foundation (T.L). The technical assistance in the statistical analyses by Ville Aalto and Irina Lisinen is acknowledged. ; Peer Reviewed
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In einer Welt, die sich zunehmend der Wichtigkeit des Umweltschutzes bewusst wird, ist es an der Zeit, über ein Thema zu sprechen, das nicht nur unsere Ökosysteme betrifft, sondern auch tiefergreifende soziale Ungerechtigkeiten aufdeckt. Wir sind alle Zeugen und Verursacher des Klimawandels und seiner verheerenden Auswirkungen. Nun wollen wir genauer hinsehen und verstehen, wie dieser Wandel bestimmte Gemeinschaften in unverhältnismäßigem Maß betrifft. Die Rede ist von Umweltrassismus.Im Folgenden soll gezeigt werden, dass Umweltprobleme nicht gleichmäßig auf alle Bevölkerungsgruppen verteilt sind, sondern oft die treffen, die bereits benachteiligt sind. Dafür wird zuerst der Begriff Umweltrassismus aus verschiedenen Perspektiven betrachtet. Anschließend wird an Beispielen genauer aufgezeigt, was für Arten es gibt, bevor es um Lösungsvorschläge gehen wird.In dem Beitrag wird von BIPoC gesprochen. BIPoC steht für "Black, Indigenous and People of Colour". Das Akronym setzt sich also aus politischen Selbstbezeichnungen von Menschen zusammen, die von rassistischer Unterdrückung betroffen sind.Ursprung des Begriffs "Umweltrassismus"?Dass die Folgen des Klimawandels immer verheerender werden, ist nichts Neues. Und dass dies enorme Gesundheitsfolgen mit sich bringt, ist auch bekannt. Dabei wird zwischen direkten (primären) Folgen und indirekten (sekundären und tertiären) Folgen unterschieden. Zu den direkten Folgen zählen eine erhöhte Sterbe- und Erkrankungsrate durch Ereignisse wie Hitzewellen, Überschwemmungen oder Waldbränden. Zu den indirekten Folgen gehören Auswirkungen wie Nahrungsmittelknappheit, Zunahme von Infektionskrankheiten und Allergien. Außerdem gibt es sozial bedingte Folgen, beispielsweise Hungersnöte, Entwicklungsstagnation oder Kriege (Kuehni, Egger 2012, S. 190). Doch was ist, wenn Teile der Erde oder bestimmte Gruppen schlimmer unter den Folgen des Klimawandels leiden als andere? In diesem Zusammenhang wird mittlerweile immer häufiger von "Umweltrassismus" gesprochen.Der Begriff kam Anfang der 1980er Jahre auf. Damals suchte der Bundesstaat North Carolina einen Ort, an dem man mit Polychlorierte Biphenylen (PCB) verseuchte Erde entsorgen kann. Zuerst war eine Entsorgungsdeponie in einem Bezirk mit hauptsächlich weißen Menschen geplant. Eine Bürgerinitiative verhinderte dies. Daraufhin war schnell klar, dass die Deponie in einem der Bezirke mit hauptsächlich schwarzen, armen oder anderweitig benachteiligten Nachbarschaften errichtet werden sollte.1982 wurde beschlossen, die verseuchte Erde in einer kleinen Gemeinde namens Afton zu entsorgen. Diese Stadt liegt in Warren County, dem damals ärmsten Landkreis in North Carolina mit einem schwarzen Bevölkerungsanteil von 65 %. Die Bevölkerung versuchte dagegen anzugehen. Zuerst gerichtlich, doch als das nichts half, gab es über sechs Wochen Sitzblockaden, Straßensperren und Demonstrationen. Dabei wurden mehr als 500 Demonstrierende verhaftet. Doch alle Bemühungen halfen nichts. Die Mülldeponie wurde dennoch gebaut. (Ituen/Tatu Hey 2021, S. 4-5). Kurz darauf wurde PCB weltweit verboten, da es sich als hochgiftig, krebserregend und erbgutschädigend herausstellte (Warda 2020).Trotz der Niederlage bei dem Bau der Deponie waren diese Proteste von großer Bedeutung und wurden von vielen anderen als Vorbild genommen. Aus Kämpfen gegen diese Art von Umweltrassismus ist schließlich die Bewegung für Klimagerechtigkeit hervorgegangen, welche erstmals Fragen sozialer Gerechtigkeit im Zusammenhang mit umweltpolitischen Aspekten betrachtete (FARN, o.J.). Geprägt wurde der Begriff Umweltrassismus von dem Bürgerrechtler Dr. Benjamin F. Chavis Jr., der an den Demonstrationen in Afton beteiligt war. Er definiert Umweltrassismus als"the intentional siting of polluting and waste facilities in communities primarily populated by African Americans, Latines, Indigenous People, Asian Americans and Pacific Islanders, migrant farmworkers, and low-income workers" (Ihejirika 2023)Chavis veröffentlichte im Jahr 1987 gemeinsam mit der United Church of Christ (UCC) Kommission eine Studie zum Thema "Toxic Wastes and Race in the United States". Aus der Studie ging hervor, dass drei von fünf BIPoC nahe einer Giftmülldeponie wohnen. In einem Dokumentarfilm sagte Davis:"The issue of environmental racism is an issue of life and death. It is just not an issue of some form of prejudice where someone doesn't like you because of the color of your skin. This is an issue that will take your life away, if you don't get involved." (United Church of Christ 2023 / o.J.).Die Protestaktion und der Film löste eine nationale Debatte über Umweltrassismus aus (United Church of Christ 2023). Die Studie von 1987 wurde bis 2007 fortgesetzt und zeigte, dass nach wie vor eine Ungleichheit herrscht und Menschen aufgrund ihrer Hautfarbe einem höheren Risiko von umweltschädlichen Stoffen ausgesetzt sind. Noch immer werden Mülldeponien eher an Standorten mit einem hohen Anteil an BIPoC erbaut, als dort, wo weiße Menschen leben (Bullard et. al. 2007, S. 155).Seither gibt es immer mehr Studien zu Umweltrassismus. Diese bestätigen, dass PoC viel stärker Umweltrisiken ausgesetzt sind als weiße Personen. Die Ursache liegt vor allem darin, dass die Industrie sich meistens dort ansiedelt, wo hauptsächlich BIPoC leben. Deshalb sind schwarze Menschen 1.5 Mal, Hispanics 1.2 Mal und einkommensschwache Menschen 1.3 Mal so viel Feinstaub ausgesetzt wie weiße Menschen bzw. einkommensstarke (Warda 2020). Durch die Studien und Veröffentlichungen zum Thema Umweltrassismus hat sich der Begriff weiterentwickelt. Der amerikanische Soziologe Robert Bullard definiert ihn als"any policy, practice or directive that differentially affects or disadvantages (where intended oder unintended) individuals, groups or communities based on race or color" (Batiste 2022, S. 1).Das Projekt "ENRICH" (Environmental Noxiousness, Racial Inequities, and Community Health) unterscheidet zwei Bestandteile des Umweltrassismus. Zum einen gibt es die räumliche Verteilungsungerechtigkeit, die sich auf die Standortwahl industrieller Umweltverschmutzer und anderer umweltgefährdender Projekte bezieht. Zum anderen handelt es sich um die Verfahrensungerechtigkeit. Dabei stehen die institutionellen Mechanismen und Richtlinien im Mittelpunkt, welche die Ungerechtigkeit aufrechterhalten (ENRICH o.J.).Umweltrassismus, Klimawandel und Kolonialismus Durch den Klimawandel werden weitere, ganz neue Seiten von Umweltrassismus aufgezeigt. Die Ursachen und Folgen des Klimawandels sind ungleich über den Planeten verteilt. Länder im globalen Süden sind meist viel stärker von den Auswirkungen des Klimawandels betroffen. Und das, obwohl sie deutlich weniger CO2-Emissionen erzeugen als der globale Norden (Warda 2020). Das zeigt, dass die Klimakrise die (globale) soziale Krise und somit den Umweltrassismus in großen Dimensionen enorm beeinflusst. Um dieses Ungleichgewicht von Nord- und Südkugel, welches mit dem Klimawandel einhergeht, zu erfassen, muss der Kolonialismus berücksichtigt werden.Im Zuge der Kolonialisierung kam es zu neuartigen globalen Handels- und Machtbeziehungen, welche bis heute anhalten. Dadurch blühte der globale Norden auf und erreichte Reichtum und Wohlstand (Bendix 2015, S. 273). Die Länder des globalen Südens galten als "Ressourcen- und Absatzmärkte" und halfen den Ländern auf der Nordhalbkugel, ihren Reichtum zu vermehren (Öztürk 2012, S. 2).Viele westliche Firmen wollen günstig in ärmeren Ländern produzieren. Meist haben die ärmeren Länder zudem eine fragile staatliche Struktur. Westliche Länder und Firmen nutzen dies aus und verschmutzen dadurch dort vor Ort die Natur und achten wenig auf Einheimische (Warda 2020). Der globale Süden wird ausgebeutet und leidet unter den massiven Eingriffen in deren Ökosysteme von außerhalb (Ziai 2012, S. 23).Aktuell zeigt sich eine erhebliche Diskrepanz im durchschnittlichen Pro-Kopf-Ausstoß von Emissionen zwischen den ärmsten Ländern, zu welchen Niger, Somalia und die Zentralafrikanische Republik gehören. Dieser Ausstoß ist in den ärmsten Ländern mehr als 140 Mal niedriger als beispielsweise in Deutschland. Dazu kommt die historische Verantwortung des Globalen Nordens hinsichtlich des Klimawandels. Der größte Teil der Emissionen, der sich seit Beginn der Industrialisierung in der Atmosphäre gesammelt hat, geht auf den Globalen Norden zurück (Kurwan 2023).Eine interessante Abbildung zu den Pro-Kopf-CO2-Emissionen im Jahr 2021 findet ihr hier. Dort wird der durchschnittliche Verbrauch von fast jedem Land dargestellt. Durch Klicken auf das Land kann man sehen, dass zum Beispiel Deutschland einen durchschnittlichen Pro-Kopf-Verbrauch an Emissionen von 8.09 hatte. Eine klare Nord-Süd Trennung der Welt ist erkennbar.Damals wie auch heute sind die Länder im globalen Süden zudem stark von der Landwirtschaft abhängig. Ihre Existenz steht babei auf dem Spiel. Um sich vor den Auswirkungen zu schützen, fehlt den Menschen, aber auch den Ländern, oftmals das Geld. Von außerhalb kommt wenig Hilfe und das, obwohl der Klimawandel ein globales Problem ist. Dennoch gibt es auf politischer Ebene einen einseitigen Fokus, welcher nur auf den vergleichsweise geringen Auswirkungen auf den globalen Norden liegt. Die Länder des globalen Südens werden mit den schlimmen gesellschaftlichen und ökologischen Folgeschäden nahezu allein gelassen.Das bedeutet nicht, dass einzelne Personen, welche die Entscheidungen treffen, eine konkrete diskriminierende Absicht haben (Bellina 2022, S. 64), aber dass viele die globalen Konsequenzen außen vor lassen und nicht bedenken. Die Folge? Sie müssen fliehen. Menschen können aufgrund der Probleme, die durch den Klimawandel ausgelöst werden, nicht in ihrer Heimat bleiben (Warda 2020).Laut einem Bericht des Internal Displacement Monitoring Centre (iDMC) aus dem Jahr 2015 verlassen seit 2008 jedes Jahr durchschnittlich 26.4 Mio. Menschen, ihre Heimat aufgrund von Naturkatastrophen. Das ist eine Person pro Sekunde. Die Zahl der geflohenen Personen sollen sich in den nächsten Jahren vervielfachen. Hauptursachen hierbei sind wetterbedingte Katastrophen wie Stürme, Überschwemmungen und Sturmfluten. Zu eher schleichenden Umweltproblemen wie Dürren oder dem ansteigenden Meeresspiegel gibt es (noch) keine konkreten Zahlen. Das sind deutlich mehr Personen, die aufgrund von Naturkatastrophen fliehen müssen, als aufgrund von Krieg. Oft stehen Umweltkatastrophen mit anderen Konflikten im Zusammenhang, beispielsweise Wasserknappheit (Yonetani 2015, S. 8). Umweltrassismus beeinflusst also das reale Überleben dieser Menschen.Doch nicht nur zwischen Süd und Nord gibt es Unterschiede. Auch die Einkommensunterschiede innerhalb eines Landes tragen dazu bei. So treffen die Folgen des Klimawandels die Menschen mit weniger Einkommen oft härter. Zum einen, weil sie weniger Wohnraum und somit weniger Rückzugsorte haben, zum anderen haben Einkommensschwache meist auch kein Auto oder eine andere Möglichkeit, am Straßenverkehr teilzunehmen und vor der Katastrophe zu fliehen (Adick 2022).Es kann auch Diskriminierung zwischen Geschlechtern und Generationen geben. Besonders Frauen und Kinder sind von den Folgen der Klimakrise betroffen (Kurwan 2023). Und das, obwohl Männer durchschnittlich mehr zur Klimaerwärmung beitragen als Frauen. Ein Grund dafür ist, dass Warnungen bei Naturkatastrophen größtenteils im öffentlichen Raum stattfinden, Frauen sich allerdings eher zuhause aufhalten und sich dort um Kinder und Haushalt kümmern und darum erst später davon erfahren. Sie sind auch bei der Flucht für Kinder und die Pflege der älteren Angehörigen zuständig (DGVN 2016). Ein weiterer Grund ist gerade bei Flutereignissen, dass Frauen seltener schwimmen können und schlechteren Zugang zu Verkehrsmitteln haben (Kurwan 2023).Eine Folge von Umweltkatastrophen, die nichts direkt mit Umweltrassismus zu tun hat, möchte ich dennoch nicht unerwähnt lassen. Laut Studien steigt die Anzahl der gewaltsamen Übergriffe auf Frauen nach Umweltkatastrophen enorm. Oftmals verdoppeln sich die Zahl der Gewalttaten von Männern gegenüber Frauen. Warum das konkret nach Katastrophen häufiger auftritt, hängt wahrscheinlich mit den fehlenden Strukturen im Chaos zusammen. Frauen sind dadurch weniger geschützt (DGVN 2016).Umweltrassismus kann also gegen einzelne Personen, Gruppen oder auch Länder auftreten. Aus den Kämpfen gegen Umweltrassismus erfolgten verschiedene Bewegungen für Klimagerechtigkeit. Einige sind uns allen bekannt, wie "Fridays for Future". Sie setzen sich nicht nur für Klimapolitik und Klimaschutz ein, sondern auch für Klimagerechtigkeit, wodurch dem Umweltrassismus entgegengewirkt werden soll (Fridays for Future 2020). Es handelt sich dabei also nicht nur um eine Klimabewegung, sondern um eine Klimagerechtigkeitsbewegung.FallbeispieleUm noch deutlicher zu zeigen, was für Arten von Umweltrassismus es auf der Erde gibt und wie oft diese auftreten, werden im Folgenden einige Beispiele aufgeführt.Das erste Beispiel handelt von den USA, genauer gesagt von den Gemeinden eines über 130 km langen Landstrichs entlang des Mississippi von Baton Rounge bis New Orleans in Louisiana. Hier haben sich insgesamt über 150 Ölraffinerien, Kunststofffabriken und andere chemische Anlagen angesiedelt, die viele Emissionen ausstoßen. Und das direkt an den zuvor bestehenden Siedlungen. Gleichzeitig weist der Abschnitt eine sehr hohe Inzidenz- und Sterblichkeitsrate im Vergleich zum Rest der USA auf. Auch die Krebsrate ist viel höher als im Rest des Landes. Aufgrund dessen wird dieser Abschnitt auch "Cancer Alley", die Allee der Krebskranken, genannt. In kaum einem anderen Bundesstaat ist die Luft so schlecht wie in Louisiana (Batiste 2022, S. 1).Doch nicht alle Menschen am Mississippi sind gleichermaßen betroffen. Vor allem die hier lebenden schwarzen Menschen auf der einen Seite des Flusses kämpfen gegen den Krebs. Verantwortlich dafür wird die Industrie gemacht. Auf der anderen Seite des Flusses leben hauptsächlich weiße Menschen, oftmals derselben Gemeinde. Aufgrund von Protesten wurden dort keine Industrieanlagen erbaut. Diese sehen die Industrie mittlerweile als Chance für neue Arbeitsplätze und Steuereinnahmen. Aber nur, wenn sie in einem bestimmten Abstand erbaut werden. Studien haben gezeigt: Je näher die Menschen an den Industrieanlagen wohnen, desto höher das Gesundheitsrisiko. Und da sich die Industrie hier auffällig nahe in Nachbarschaften mit hauptsächlich BIPoC oder Armen angesiedelt haben, gehen diese von einem rassistischen Motiv aus. Sie haben das Gefühl, geopfert zu werden, an zweiter Wahl zu stehen (Schmidt 2023).Eine Studie aus den USA zeigt, dass es eine besonders hohe Sterberate bei BIPoC gibt im Zusammenhang mit Hitzewellen. Vor allem in Großstädten sterben doppelt so viele wie weiße Menschen. Das liegt an den Temperaturdifferenzen innerhalb der schwarzen und weißen Nachbarschaft, welche bei bis zu 1.7° Celsius liegen kann (Ituen/Tatu Hey 2021, S. 12/13).Doch Umweltrassismus gibt es auch in Deutschland. So wurde durch verschiedene Studien festgestellt, dass es beispielsweise in Kassel eine erhöhte Luftverschmutzung in den Bezirken gibt, in welchen Menschen mit niedrigen sozioökonomischen Status und Migrationshintergrund wohnen (Ituen/Tatu Hey 2021, S. 9). Auch andere marginalisierte Gruppen, wie Sinti*zza und Rom*nja erleben dies immer wieder. Meistens werden sie in Gegenden mit einer hohen Umweltbelastung geschoben und von Umweltgütern wie sauberem Trinkwasser ausgeschlossen (Ituen/Tatu Hey 2021, S. 8).Eine neue Studie aus Chicago verdeutlicht, dass Schwarze während der Pandemie für 50 % der Corona-Infektionen und sogar 70 % der Todesfälle verantwortlich waren. Und das, obwohl sie lediglich 30 % der Bevölkerung von Chicago ausmachen. Und auch in Großbritannien zeigt sich, dass schwarze Menschen fast doppelt so häufig wie weiße Menschen einem erhöhten Risiko ausgesetzt sind, an Covid-19 zu sterben (Ituen/Tatu Hey 2021, S. 13).Ebenso können ganze Länder von Umweltrassismus betroffen sein, wie beispielsweise Senegal. Der globale Süden ist durch Kolonialisierung und jahrhundertelange Ausbeutung viel später in die Industrialisierung eingestiegen. Bis dahin haben die Länder des Nordens schon viel, viel mehr CO2 ausgestoßen, welches über 100 Jahre in der Atmosphäre bleibt. Trotzdem sollen die Länder des globalen Südens genau so viel CO2 einsparen wie die Länder auf der Nordhalbkugel. Gleichzeitig sollen sie die Schulden gegenüber dem globalen Norden abbauen. Das führt dazu, dass Länder im Süden (z.B. Senegal) ihre fossilen Energieträger von Industrienationen ausbeuten lassen, um nicht noch tiefer in die Schulden zu stürzen (Adick 2022).Umweltrassismus bekämpfenDie Bekämpfung von Umweltrassismus wird von Land zu Land unterschiedlich gehandhabt. Der gemeinsame Kern ist jedoch, dass das Leid der betroffenen Personen gemindert werden soll. Diese wollen auf sich aufmerksam machen und gegen das Unrecht ankämpfen. So war es auch bei Cancer Alley. Gemeinsam mit Anwälten wurden Klagen gegen staatliche Einrichtungen oder chemische Fabriken angestrengt (Schmidt 2023). Robert Taylor, der Gründer der Initiative gegen die Chemiefabriken, kämpft für eine bessere Zukunft. Vor allem für die BIPoC-Kinder der Gemeinden. Weitere Forderungen sind Verschärfungen von Vorschriften der EPA (Envioronmental Protection Agency), welche eine unabhängige Behörde der USA ist und sich für den Umweltschutz und den Schutz der menschlichen Gesundheit einsetzt, und eine Wiedergutmachung für die betroffenen und hinterbliebenen Personen (Batiste 2022, S. 29).Mittlerweile hat auch Präsident Joe Biden davon gehört und Taylor ins Weiße Haus eingeladen. Hier soll er verdeutlichen, dass Umweltschutz oberste Priorität hat und somit auch dem Umweltrassismus entgegengewirkt werden kann. Es gibt den Anwohner*innen und Umweltgruppen Hoffnung. Außerdem verlangen sie mehr Forschung zu dem Thema, um besser ihr Leid belegen zu können. Sie glauben, dass die Politik ihnen dann mehr Glauben schenkt (Schmidt 2023). Die daraus resultierende nationale Aufmerksamkeit soll der Wendepunkt von Cancer Alley sein (Batiste 2022, S. 29).Ein weiteres einzigartiges und innovatives Projekt wurde 2012 von Dr. Ingrid Waldron in Kanada ins Leben gerufen. Dabei handelt es sich um das sogenannte ENRICH-Projekt (Environmental Noxiousness, Racial Inequities, and Community Health), welches sich auf die sozialen, ökologischen, politischen und gesundheitlichen Auswirkungen von Umweltrassismus in Mi´kmaq-Gemeinden (Ureinwohner*innen) und Nova Scotia, einer kleinen Provinz in Kanada, spezialisieret (ENRICH o.J.). Die hauptsächlich dort lebenden BIPoC berichten von Krankheiten wie Krebs oder Diabetes, welche aufgrund von Mülldeponien, die 1974 und 2006 eröffnet wurden, hervorgerufen wurden. Außerdem hatten sie kaum Zugang zu sauberem Trinkwasser, da das Wasser viele Giftstoffe enthielt. Der Müll zog zudem Bären, Waschbären und Insekten an (Klingbeil 2016).Das Projekt will Wege finden, um räumliche wie verteilungstechnische Arten des Umweltrassismus in diesen Gemeinden anzugehen und mithilfe der Bürger*innen die Politik bzw. Politiker*innen zum Handeln zu zwingen. Des Weiteren wollen sie national über die Ansiedlung und Regulierung von Industrieanlagen im Zusammenhang mit Umweltrassismus informieren. Das machen sie mithilfe von Interessenvertretungen, gemeinschaftlichem Engagement, Mobilisierung und Kapazitätsaufbau in betroffenen Gemeinden, öffentlicher Bildung, Studierendenausbildung, sektorübergreifenden Partnerschaften, Workshops und Kommunikation (ENRICH o.J.). Auch ihnen ist es in erster Linie wichtig, auf diese Umstände aufmerksam zu machen. Die Beteiligten schafften es, dass im Jahr 2015 zum ersten mal in Kanada ein Gesetzesentwurf zum Thema Umweltrassismus eingebracht und bis zur zweiten Lesung durchgebracht wurde. Allerdings wurde das Gesetz nicht verabschiedet (Klingbeil 2016).Das Projekt sorgte weltweit für Aufsehen. Im April 2018 veröffentlichte Waldron das Buch "There´s something in the water" und verwendete Nova Scotia als Fallbeispiel, um die Auswirkungen von Umweltrassismus und dessen gesundheitliche Folgen auf indigene und schwarze Gemeinschaften in Kanada zu untersuchen. Das Buch erhielt zwei Preise. 2019 wurde der gleichnamige Dokumentarfilm veröffentlicht.Das sind einzelne Projekte, die wichtig sind und von denen Betroffene profitieren können. Jedoch können sie nicht dem globalen Umweltrassismus entgegenwirken, welcher heute enorme Dimensionen angenommen hat. Nicht nur Bevölkerungsgruppen, sondern auch Länder sind unterschiedlich von den Folgen des Klimawandels betroffen. Die Politik kann und muss dagegen ankämpfen. Es gibt schon Lösungsideen, wie dem Umweltrassismus entgegengewirkt werden kann.Ein Prinzip, das dabei beachtet werden sollte, ist das Verursacherprinzip. Dabei sollen nicht nur die aktuellen Emissionen berücksichtigt werden, sondern auch die historische Verantwortung. Das bedeutet, dass beachtet werden muss, welches Land wie viel CO2 in der Vergangenheit ausgestoßen hat. Dadurch verändert sich das CO2-Budget der Länder im Norden. Teilweise wäre das Budget schon komplett aufgebraucht. Außerdem sollen die Nationen des globalen Nordens die Verantwortung als hauptsächliche Verursacher des Klimawandels auf sich nehmen und für die Kosten von Anpassungsstrategien und klimabedingten Schäden in Ländern des globalen Südens aufkommen müssen (Kurwan 2023).Eine weitere Lösung, die das Problem beheben könnte, ist ein Schuldenerlass. Das führt dazu, dass fossile Energieträger des globalen Südes im Boden bleiben können und die Länder das Geld anders investieren können. Beispielsweise in eine Veränderung, die sozial und ökologisch gerecht wäre. Des Weiteren könnten sie mit dem Geld die Klimaanpassung (mit-)finanzieren. Viele Wissenschaftler*innen oder auch der Internationale Währungsfonds (IWF) haben sich positiv zu dieser Lösung geäußert. Somit könnte den ärmeren Ländern mehr finanzieller Spielraum gegeben werden. Das kann ein Hilfsmittel gegen die Ungerechtigkeit sein. Jedoch kann es diese nicht komplett lindern. Der Norden muss definitiv noch mehr investieren. Denn wie schon weiter oben gesagt, hängt die Klimakrise eng mit der sozialen Gerechtigkeit und somit dem Umweltrassismus zusammen.FazitDer Beitrag beleuchtete das komplexe Thema des Umweltrassismus. Der Begriff wurde Anfang der 1980er Jahre geprägt und bekommt immer mehr Bedeutung. Umweltrassismus hat viele Facetten. Es tritt auf, wenn Umweltprobleme und Umweltverschmutzung unverhältnismäßig stark bestimmte Gemeinschaften betreffen. Meist betrifft es die Menschen, die bereits benachteiligt sind.Umweltrassismus ist also nicht nur eine Frage der Umwelt, sondern auch eine der sozialen Gerechtigkeit, wenn nicht sogar eine Frage von Leben und Tod. Neben BIPoC können auch Geschlechter und Generationen sowie ganze Länder direkt oder indirekt betroffen sein. Häufig trifft es Frauen, Kinder und Einkommensschwache am stärksten.Der globale Norden, der historisch für einen Großteil der CO2-Emissionen verantwortlich ist, leidet weniger unter den Folgen des Klimawandels als der globale Süden. Und das, obwohl der Süden deutlich weniger Emissionen verursacht.Um dem Umweltrassismus entgegenzuwirken, gibt es verschiedene Lösungsansätze. Diese reichen von gemeindebasierten Initiativen und internationaler Zusammenarbeit bis hin zu Gerichtsverfahren und politischen Maßnahmen. Ein wichtiger Schritt dabei ist es, die historische Verantwortung anzuerkennen und den globalen Norden zur Verantwortung zu ziehen. Ein Schuldenerlass für die Länder des globalen Südens könnte ihnen zudem finanzielle Ressourcen verschaffen, die sie in umweltfreundliche Technologie stecken können.Mit diesem Beitrag soll ein Bewusstsein für Umweltrassismus geschaffen werden. Das Ziel ist es, dass weniger CO2 freigesetzt wird, um eine nachhaltige Welt zu schaffen, in der Umweltressourcen und Chancen fair verteilt werden und niemand aufgrund seiner Hautfarbe oder seines sozialen Status benachteiligt wird. Es erfordert Engagement auf individueller und globaler Ebene, um die notwendigen Veränderungen herbeizuführen.LiteraturverzeichnisAdick, Katharina (2022): SPEZIAL: Klimagerechtigkeit – So wird Klimaschutz sozialer (Audio-Podcast). 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A Report Prepared for the United Chruch of Christ Justice & Witness Ministeries. < http://d3n8a8pro7vhmx.cloudfront.net/unitedchurchofchrist/legacy_url/7987/toxic-wastes-and-race-at-twenty-1987-2007.pdf?1418432785 > (27.09.2023).Deutsche Gesellschaft für die Vereinten Nationen (DGVN) (2016): Klimagerechtigkeit und Geschlecht: Warum Frauen besonders anfällig für Klimawandel & Naturkatastrophen sind. < https://dgvn.de/meldung/klimagerechtigkeit-und-geschlecht-warum-frauen-besonders-anfaellig-fuer-klimawandel-naturkatastroph > (30.09.23).Environmental Noxiousness, Racial Inequities, and Community Health (ENRICH): Welcome to the ENRICH Project < https://www.enrichproject.org/ > (28.09.23).Fachstelle Radikalisierungsprävention und Engagement im Naturschutz (FARN) (o.J.): Von Umweltrassismus zu Klimagerechtigkeit? Koloniale Kontinuitäten in der Klimakrise. < https://www.nf-farn.de/umweltrassismus-klimagerechtigkeit-koloniale-kontinuitaeten-klimakrise > (28.09.23). 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S. 187-194.Kurwan, Jenny (2023): Klimagerechtigkeit. < https://www.bpb.de/themen/klimawandel/dossier-klimawandel/515255/klimagerechtigkeit/ >Öztürk, Asiye (2012): Editorial. In: Aus Politik und Zeitgeschichte. Kolonialismus. (44-45). S. 2Schmidt, Sarah (2023): Krebskrank am Öl-Delta. < https://www.tagesschau.de/ausland/amerika/krebs-diskriminierung-usa-100.html > (30.09.23).United Church of Christ (2023): A Movement Is Born: Environmental Justice and the UCC. < https://www.ucc.org/what-we-do/justice-local-church-ministries/justice/faithful-action-ministries/environmental-justice/a_movement_is_born_environmental_justice_and_the_ucc/ > (27.09.2023).Warda, Johanna (2020): Ist der Klimawandel rassistisch? Die einen produzieren die Klimakatastrophe, die anderen baden sie aus – diese Annahme beschreibt der Begriff "Klimarassismus". Woher kommt er und was ist dran? < https://www.fluter.de/klimawandel-ist-ungerecht-verteilt > (27.09.2023).Yonetani, Michelle (2015): Global Estimates 2015. People displaced by disasters. < https://www.internal-displacement.org/sites/default/files/inline-files/20150713-global-estimates-2015-en-v1.pdf > (27.09.2023).Ziai, Aran (2012): Neokoloniale Weltordnung? In: Aus Politik und Zeitgeschichte. Kolonialismus. (44–45). S. 23-30.
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Exakt 20 Jahre nach den Terroranschlägen vom 11. September 2001 kündigte der derzeit amtierende US-Präsident Joe Biden den Abzug aller amerikanischen Truppen aus Afghanistan an. "Es ist Zeit, Amerikas längsten Krieg zu beenden" (Böhm 2021, 92). Bereits vor dem Einmarsch amerikanischer und britischer Truppen am 7. Oktober 2001, bekannt als die Operation "Enduring Freedom", hatte Amerika Stützpunkte der in Afghanistan ansässigen Terrorgruppe Al-Qaida attackiert. Der Grund hierfür waren die durch Mitglieder der Gruppe geplanten und durchgeführten Anschläge auf amerikanische Botschaften in Tansania und Kenia im Jahr 1998. "Aber die Schwelle der Kriegserklärung gegen Terroristen wurde nicht überschritten, auch um Letztere politisch nicht aufzuwerten" (Böhm 2021, 94).Als Wendepunkt gilt der 11. September 2001. Neunzehn Terroristen der Terrorgruppe Al Qaida entführten vier Passagierflugzeuge. Zwei dieser Flugzeuge wurden in die Twin Towers des World Trade Centers gesteuert. Ein weiteres zerstörte den westlichen Teil des Pentagons in Washington. Das vierte stürzte in einem Feld in New Jersey ab. Insgesamt starben durch diese vier Flugzeuge fast 3000 Menschen aus 80 verschiedenen Ländern (vgl. Hoffmann 2006, 47).Die Anschläge veränderten die Wahrnehmung der durch den Terrorismus bestehenden Bedrohung. Bereits wenige Tage nach den Anschlägen verkündete der damalige US-Präsident George W. Bush den "Global War on Terror" (Böhm 2021, 92), eine Kriegserklärung an den Terrorismus. Damit definierte er die Auseinandersetzung mit dem Terrorismus als Krieg.Neben dieser Auslegung gilt auch die Interpretation des Verhältnisses zwischen terroristischen Gruppierungen und Amerika feindlich gesinnten Staaten als entscheidend. Unmittelbar nach den Anschlägen wurde zunächst nur die Bekämpfung der Terrorgruppe Al-Qaida und des Taliban-Regimes in Afghanistan priorisiert. In den darauffolgenden Monaten wurden neben diesen auch den Terrorismus unterstützende, autoritäre Staaten und Staaten mit Zugang oder Beschaffungsmöglichkeiten von Massenvernichtungswaffen zu möglichen Zielen von Militäraktionen zur Bekämpfung des Terrorismus (vgl. Böhm 2021, 92; Kahl 2011, 19).Durch die Anschläge am 11. September 2001 wurde neben der "seit längerem bekannte Dimension der internationalen Kooperation von terroristischen Gruppen […] die neue Dimension der transnationalen Kooperation, Durchführung, Logistik und Finanzierung terroristischer Gewalt deutlich" (Behr 2017, 147).Im Rahmen dieses Beitrags wird der Terrorismus als eine Herausforderung für die Vereinten Nationen vor und nach den Anschlägen vom 11. September 2001 thematisiert. In diesem Zusammenhang wird der Frage nachgegangen, inwiefern diese die Sicherheitspolitik der Vereinten Nationen beeinflusst haben. In einem ersten Schritt wird eine Klärung des Begriffs Terrorismus vorgenommen. Im Anschluss daran wird auf die Strategien der Vereinten Nationen zur Bekämpfung des Terrorismus vor dem 11. September 2001 eingegangen. Darauf folgt eine Darstellung der direkten Reaktionen der internationalen Staatengemeinschaft auf die Anschläge. In einem letzten Schritt werden die daraus resultierenden Folgen für die internationale Sicherheitspolitik näher beleuchtet.BegriffsklärungIn einem ersten Schritt gilt es nun, den Begriff des Terrorismus näher zu definieren. Der Begriff leitet sich von dem lateinischen Wort terror ab, das als Schrecken oder Furcht übersetzt werden kann (vgl. Pfahl-Traughber 2016, 10). Nach dem Terrorismusexperten Bruce Hoffmann wird unter dem Begriff des Terrorismus die "bewusste Erzeugung und Ausbeutung von Angst durch Gewalt oder die Drohung mit Gewalt zum Zweck der Erreichung politischer Veränderung" (Hoffmann 2006, 80) verstanden.Dementsprechend ist eine terroristische Tat zunächst einmal gekennzeichnet durch die Androhung oder die Ausübung von Gewalt. Im Hinblick auf die Intensität der ausgeübten Gewalt wird deutlich, dass keine humanitären Konventionen respektiert werden und terroristische Anschläge sich oft durch "besondere Willkür, Unmenschlichkeit und Brutalität" (Waldmann 2005, 14) auszeichnen."Die Gewalttat hat primär einen symbolischen Stellenwert, ist Träger einer Botschaft, die in etwa lautet, ein ähnliches Schicksal kann jeden treffen, insbesondere diejenigen, die den Terroristen bei ihren Plänen im Wege stehen" (Waldmann 2005, 15). Basierend auf dieser Tatsache bezeichnet der Soziologe Peter Waldmann den Terrorismus "primär [als] eine Kommunikationsstrategie" (Waldmann 2005, 15).Auf der psychologischen Ebene verfolgt der Terrorismus das Ziel, über die unmittelbaren Ziele und Opfer hinaus bei einer bestimmten Gruppe Furcht hervorzurufen, um für deren Einschüchterung zu sorgen. Als Zielgruppe kommt neben Staaten, Regierungen und einzelnen religiösen oder ethnischen Gruppen auch die allgemeine öffentliche Meinung in Frage (vgl. Hoffmann 2006, 80).Davon ausgehend verfolgt der Terrorismus mit der Erzeugung von Furcht und Schrecken auf der politischen Ebene das Ziel, das Vertrauen in eine bestehende politische Ordnung zu erschüttern (vgl. Waldmann 2005, 16). Im Hinblick auf die politische Dimension des Terrorismus grenzt Waldmann diesen bewusst vom Staatsterrorismus ab. Nach Waldmann kennzeichnen terroristische Anschläge ihre planmäßige Vorbereitung und ihre Aktivität aus dem Untergrund heraus.Im Gegensatz dazu handelt es sich bei Staatsterrorismus um ein Terrorregime, errichtet durch staatliche Machteliten. Von Seiten des Staates kann zwar Terror gegenüber seinen Bürgern ausgeübt werden, er ist jedoch nicht in der Lage, die genannten Strategien gegen die eigene Bevölkerung einzusetzen (vgl. Pfahl-Traughber 2016, 17; Waldmann 2005, 12).Bei den Akteuren handelt es sich um einen Zusammenschluss von Handlungswilligen, die sich in annähernd bürokratischen Strukturen organisieren, wobei Hierarchien und informelle Abhängigkeiten entstehen. In den meisten Fällen verfügen diese Gruppierungen über eine "geringe quantitative Dimension […] handelt es sich doch überwiegend um kleinere Personenzusammenschlüsse von wenigen Aktivisten" (Pfahl Traughber 2016, 12).Diese agieren im Untergrund, da sie weder über den erforderlichen Rückhalt innerhalb einer Bevölkerung noch über die erforderliche Kampfstärke verfügen. Am Beispiel von Al-Qaida in Afghanistan wird deutlich, dass ein Hervortreten aus dem Untergrund, beispielsweise durch die Errichtung von Lagern, das Risiko impliziert "angegriffen und vernichtet zu werden" (Waldmann 2006, 13).Hinsichtlich der Bezeichnung werden im Sprachgebrauch zwei Arten von Terrorismus, der internationale und der transnationale Terrorismus, unterschieden. In diesem Zusammenhang stellt sich die Frage, ob das Phänomen des Terrorismus eher als international oder transnational zu bezeichnen ist. Nach Steinberg zeigt sich aus historischer Sicht ein fließender Übergang von dem internationalen Terrorismus hin zum transnationalen Terrorismus.Der internationale Terrorismus zeichnet sich in erster Linie durch "zahlreiche grenzüberschreitende Aktionen [aus], bei denen häufig vollkommen unbeteiligte Bürgerinnen und Bürger fremder Staaten zu Schaden kamen." (Steinberg 2015). Ferner ist für den internationalen Terrorismus charakteristisch, dass die terroristischen Aktivitäten durch Staaten unterstützt werden. Zu den Unterstützerstaaten in der Vergangenheit zählten insbesondere Verbündete der ehemaligen Sowjetunion wie beispielsweise Syrien oder Libyen.Als historisches Beispiel für den internationalen Terrorismus gelten die Attentate auf israelische Sportler*innen während der Olympischen Spielen in München 1972 durch palästinensische Terroristen. Mit dem Fall der UdSSR verloren diese Staaten ihren Schutz vor Sanktionen westlicher Nationen. Damit endete nach und nach auch die Unterstützung terroristischer Gruppierungen. Es folgte ein fließender Übergang vom internationalen Terrorismus hin zum transnationalen Terrorismus.Der Unterschied besteht darin, dass die terroristischen Aktivitäten nicht mehr durch einen Staat unterstützt werden. Die Gruppierungen werden privat mit Geld und Waffen unterstützt oder bauen eigene, substaatliche Logistik- und Finanzierungsnetzwerke auf. Der Terrorismus gilt zudem als transnational, "weil sich die terroristischen Gruppen auf substaatlicher Ebene länderübergreifend miteinander vernetzen und sich dementsprechend aus den Angehörigen verschiedener Nationalitäten zusammensetzen" (Steinberg 2015).Basierend auf diesen Erkenntnissen ist ab den 1990er Jahren nicht mehr von internationalem Terrorismus, sondern vielmehr von transnationalem Terrorismus zu sprechen (vgl. Steinberg 2015). Dies hat auch Auswirkungen auf die Organisationsstrukturen terroristischer Gruppierungen. Sie zeichnen sich durch "Dezentralisierung, Entterritorialisierung und durch Überlagerung und Fragmentierung zwischen wechselnden, funktional orientierten Akteuren aus" (Behr 2017, 150).Ein Beispiel für den Übergang von einer internationalen Organisation hin zu einem transnationalen Netzwerk stellt die im Zusammenhang mit dem 11. September 2001 stehende Terrorgruppe Al-Qaida dar. Vor den Anschlägen galt sie als eine internationale Organisation, die über ein "recht einheitliches Gebilde" (Hoffmann 2006, 425) verfügt. In Folge der Reaktionen auf die Anschläge entwickelte sie sich als eine transnationale Bewegung "mit gleich gesinnten Vertretern an vielen Orten, die über ein ideologisches und motivierendes Zentrum locker miteinander verbunden sind, aber die Ziele dieses noch verbleibenden Zentrums gleichzeitig und unabhängig voneinander verfolgen" (Hoffmann 2006, 425).Nach Vasilache ist "der gebräuchliche Terminus des internationalen Terrorismus irreführend, da er keine gängige Strategie eines Staates gegen einen anderen, sondern ein transnationales Phänomen ist, das vor Staatsgrenzen nicht halt macht" (Vasilache 2006, 151). Als Begründung führt er an, dass terroristische Anschläge oftmals von einzelnen Gruppierungen ausgehen, wobei auf die unterschiedlichen Motive in einem nächsten Schritt eingegangen wird. Weiterhin begründet er seine Aussage mit der Tatsache, dass das Ziel von staatlich initiiertem Terrorismus nicht direkt ein anderer Staat ist, sondern vielmehr zivile Ziele verdeckt attackiert werden (vgl. Vasilache 2006, 151).Anders als Steinberg spricht Vasilache also nicht von einer historischen Veränderung vom internationalen Terrorismus hin zum transnationalen Terrorismus, sondern bezeichnet das Phänomen Terrorismus generell als transnational. Da beide in der Ansicht übereinstimmen, zum Zeitpunkt der Anschläge am 11. September 2001 handele es sich um die transnationale Form des Terrorismus, wird im weiteren Verlauf von transnationalem Terrorismus gesprochen.Im Hinblick auf die Motive terroristischer Gruppierungen können im Wesentlichen vier Motive benannt werden, die sich überschneiden oder einander angleichen können. In diesem Zusammenhang wird von der Tatsache ausgegangen, dass terroristische Gruppierungen mit ihren Zielen und ideologischen Rechtfertigungen nicht zufällig entstehen, "sondern einen bestimmten gesellschaftlich-historischen Hintergrund widerspiegelt, der seinerseits wieder durch ihr Vorgehen eine spezifische Aktivierung erfährt" (Waldmann 2005, 100).Der sozialrevolutionäre Terrorismus möchte die politischen und gesellschaftlichen Strukturen nach der Ideologie von Karl Marx verändern (vgl. Waldmann 2005, 99). Ein Beispiel hierfür stellt die Rote Armee Fraktion (kurz: RAF) dar, die in den 1970er Jahren in Deutschland terroristische Anschläge verübte.Wenn unterdrückte Völker oder Minderheiten das Ziel von mehr politischer Autonomie oder staatlicher Eigenständigkeit mit terroristischen Strategien verfolgen, handelt es sich um ethnisch-nationalistischen Terrorismus. Als Exempel hierfür kommt die baskische ETA infrage, die aus einer Studierendenorganisation heraus entstanden ist und sich in den 1960er Jahren zunehmend radikalisierte (vgl. Waldmann 2005, 103f.).Unter die dritte Form des Terrorismus, "der militante Rechtsradikalismus" (Waldmann 2005, 115), fallen unterschiedliche Gruppen wie beispielsweise die Ku-Klux-Klan-Bewegung in Amerika. Trotz der unterschiedlichen Ausprägungen können bei all diesen Gruppen im Wesentlichen zwei Merkmale ausgemacht werden: zunächst einmal kämpfen sie für den Erhalt bestehender Strukturen und wollen keine strukturellen Veränderungen hervorrufen. Zudem richtet sich diese Form des Terrorismus in erster Linie nicht gegen das politische System, sondern vielmehr gegen einzelne Gruppen der Gesellschaft (vgl. ebd., 115). Ferner kennzeichnet den rechtsradikalen Terrorismus auch eine andere Strategie und eine andere Erscheinungsform. Bei den Aktivisten handelt es sich um "Teilzeitterroristen" (ebd., 117), die typischerweise in ihrer Freizeit agieren. Ihre Aktivitäten sind nicht im Untergrund, sondern werden vielmehr offen durchgeführt. Hinzu kommt, dass die Anschläge teils geplant und teils spontan erfolgen, mit dem Ziel, die Opfer zum Verlassen des Ortes oder Landes zu bewegen (vgl. ebd., 117f.).Bei der vierten Form des Terrorismus handelt es sich um religiös motivierten Terrorismus. Beispiel hierfür ist die bereits mehrfach angesprochene Terrorgruppe Al-Qaida. Sie entstand als Reaktion auf den Angriff der Sowjetunion auf Afghanistan Ende der 1970er Jahre. Die Brutalität der Invasion sorgte für eine große Solidarität innerhalb der islamischen Welt und führte zu einem Zuzug von zahlreichen islamischen Glaubenskämpfer*innen aus anderen Ländern, darunter auch Osama Bin Laden. Dieser gewann im Laufe der 1980er Jahre immer mehr an Einfluss und gründete mit dem Abzug der Sowjets Ende des Jahrzehnts Al Qaida mit dem Ziel, an einer anderen Front weiterzukämpfen. Es erfolgte ein Strategiewechsel "des Djihads nach innen, gegen verräterische Herrscher in den islamischen Staaten, auf die Strategie eines Djihads nach außen, gegen den Westen" (ebd., 152).Ein definitorisches Problem von Terrorismus ergibt sich aus der Tatsache, dass auf der internationalen Ebene bislang keine einheitliche Definition gefunden wurde. Im Rahmen der Resolution 1566 aus dem Jahr 2004 definierte der Sicherheitsrat der Vereinten Nationen den Begriff Terrorismus wie folgt als "Straftaten […], die mit dem Ziel begangen werden, die ganze Bevölkerung, eine Gruppe von Personen oder einzelne Personen in Angst und Schrecken zu versetzten, eine Bevölkerung einzuschüchtern oder eine Regierung oder eine internationale Organisation zu einem Tun oder Unterlassen zu nötigen […]" (UN-Resolution1566 2004).Neben dieser existieren weitere nationale und internationale Definitionen, wie unter anderem die der Europäischen Union oder die Definitionen einzelner amerikanischer Behörden. Auf der politischen Ebene können die Schwierigkeiten hinsichtlich einer einheitlichen Definition anhand folgender Punkte näher beleuchtet werden: zunächst einmal werden Handlungen von unterschiedlichen Staaten unterschiedlich eingestuft. Für die einen handelt es sich um gewalttätige terroristische Angriffe; andere stufen die Aktivitäten als politisch legitimierte Handlungen in Ausübung des Selbstverteidigungsrechts während eines nationalen Befreiungskampfes ein.Ferner herrscht Uneinigkeit darüber, ob eine Definition auch den Staatsterrorismus umfassen sollte oder ob sie lediglich die motivationalen Hintergründe der Täter umfasst. Anhand der genannten Schwierigkeiten wird deutlich, dass die Einschätzung, ob es sich bei der Bedrohung um eine terroristische Bedrohung handelt und ob es sich bei der Organisation um eine terroristische Organisation handelt, dem nationalen Verständnis oder dem Verständnis der jeweiligen Institution unterliegt. Folglich könnte die Klassifizierung missbraucht werden, um ungewünschte innerstaatliche Gruppierungen oder andere mit dem Begriff zu stigmatisieren und deren Verfolgung zu rechtfertigen (vgl. Finke/Wandscher 2001, 168; Kaim 2011, 6).Abschließend gilt es noch zu klären, ob terroristische Aktivitäten als Kriegshandlungen bezeichnet werden können oder ob vielmehr eine Trennung der beiden Begriffe erforderlich ist. Als unmittelbare Reaktion auf die Anschläge des 11. Septembers bekundete Amerika immer wieder seinen Krieg gegen den Terror. Neben Präsident Bushs "global war on terror" sprach auch der amerikanische Verteidigungsminister Donald H. Rumsfeld im Zuge der Anschläge von einer neuen Kriegsart, "die sich vor allem neuer Technologien bedienen, asymetrisch verfahren und deswegen auch nicht leicht zu erkennen sein würde" (Czempiel 2003, 113).Diese Verwendung des Kriegsbegriffes in Verbindung mit terroristischen Anschlägen offenbart einen strategischen Zug der US-Regierung. "Dehnt man den Kriegsbegriff auf terroristische Akte aus, legitimiert dies den Angegriffenen auch zu Kriegshandlungen" (Geis 2006, 12). Der Regierung ist es infolgedessen möglich, über rechtsstaatliche Mittel hinaus Maßnahmen zu ergreifen und sie kann zudem von einer breiten Unterstützung innerhalb der eigenen Bevölkerung ausgehen (vgl. Geis 2006, 12). Bei der Frage, ob der transnationale Terrorismus als eine Form des Krieges bezeichnet werden kann, offenbart sich aus politikwissenschaftlicher Sicht eine erhebliche Kontroverse.Neben der Kategorisierung zwischen den alten und neuen Kriegen existiert auch die Unterscheidung zwischen großen und kleinen Kriegen. Diese "basiert auf der Art der Vergesellschaftungsform der Kriegführenden" (Geis 2006, 21). Im Fall des großen Krieges sind die Akteure in gleichem Maß vergesellschaftet, ein Staat kämpft gegen einen anderen Staat. Im Falle eines kleinen Krieges besteht eine "asymetrische Konfliktstruktur zwischen ungleich vergesellschaftlichen Akteuren: Staatliche Kombattanten treffen auf nichtstaatliche Kämpfer" (Geis 2006, 21).Ob unter die kleinen Kriege auch der Terrorismus zu subsumieren ist, ist jedoch umstritten. Zunächst einmal wird dagegen angeführt, dass der Preis auf normativer Ebene zu hoch sei. Eine Unterscheidung beider bedeutet einen Fortschritt des Völkerrechts, da die Trennung immer eine Unterscheidung zwischen politisch legitimierter Gewalt im Zuge einer Kriegshandlung und illegitimer Gewalt, ausgeübt im Zuge eines Verbrechens, ermöglicht.Hinzu kommen Bedenken "bezüglich der Folgen eines ungehegten Counterterrorismus der angegriffenen Staaten" (Geis 2006, 22). In einem permanenten Kriegszustand hätten demokratische Staaten die Möglichkeit, die Erweiterung des Sicherheitsapparates und Bürgerrechtseinschränkungen zu legitimieren (vgl. ebd., 21f.). Als weiteres Argument wird angeführt, dass eine Trennung beider Begriffe aus analytischer Sicht sinnvoll sei, da es sich beim Terrorismus primär um eine Kommunikationsstrategie handele. Dieser fehlen neben der territorialen Dimension auch die wechselseitig beständige Gewaltanwendung und das Charakteristikum eines Massenkonflikts (vgl. ebd., 23).Für eine Subsumierung des Terrorismus unter den Kriegsbegriff spricht insbesonders die Sichtweise der Vereinten Nationen, die im Zuge der Anschläge vom 11. September 2001 den Vereinigten Staaten von Amerika das Recht auf Selbstverteidigung gemäß Art. 51 UN-Charta zugesprochen hat (vgl. Resolution 1373 2001). Auf diese Tatsache wird zu einem späteren Zeitpunkt noch einmal eingegangen. Anschließend wird der Sichtweise der Vereinten Nationen gefolgt und folglich der Terrorismus unter den Begriff des Krieges subsumiert.Reaktionen der Vereinten Nationen auf Terrorismus vor dem 11. September 2001In einem nächsten Schritt gilt es, auf die Reaktionen der Vereinten Nationen auf das Phänomen des Terrorismus vor dem 11. September 2001 einzugehen. Hierbei wird zunächst auf das unterschiedliche Verständnis in Bezug auf den Sicherheitsbegriff näher eingegangen. Seit den 1970er Jahren gilt nicht mehr nur die politische Souveränität und die territoriale Integrität der einzelnen Staaten als das zu schützende Objekt der Sicherheitspolitik.Neben der zu schützenden staatlichen Sicherheit geriet auch die Gesellschaft, definiert als ein "Zusammenschluss von Individuen" (Kaim 2011, 3), in den Mittelpunkt sicherheitspolitischen Handelns. In den 1990er Jahren erfolgte die Aufnahme einer weiteren Dimension in Gestalt der menschlichen Sicherheit in den Diskurs rund um den Sicherheitsbegriff und die damit verbundenen Aufgaben. Nach diesem Verständnis ist die Sicherheit, die Freiheit und der Wohlstand des Individuums zu schützen. Es zeigt sich jedoch, dass die Dimensionen in der politischen Praxis nicht getrennt voneinander betrachtet werden können. Der Schutz des Individuums umfasst ebenso die Gesellschaft, in der es lebt, und letzlich auch den Staat (vgl. Kaim 2011, 3f.).Aus sicherheitspolitischer Perspektive gilt der "Terrorismus als entterritorialisiertes Sicherheitsrisiko" (Behr 2017, 151), das zu drei Konsequenzen führt. Zunächst einmal sind terroristische Aktivitäten nicht voraussagbar. Es besteht das Risiko, dass sie sich zu jeder Zeit an jedem Ort ereignen können. Hinzu kommt, dass die Akteure anders als Staaten keine politische Einheit darstellen. Vielmehr ereignen sich einzelne, verstreut zusammenhängende Handlungen ohne einen genau ausmachbaren Anfang oder Ende. Folglich kann auf das sicherheitspolitische Risiko Terrorismus nur reagiert werden, wenn die Maßnahmen "Handlungs- und Organisationslogiken transnationaler Politik erfassen und übernehmen" (Behr 2017, 151).Die Problematik des transnationalen Terrorismus als Herausforderung für die Vereinten Nationen und ihrer Sonderorganisationen führte zu einer Reihe von Abkommen mit der Intention der Beseitigung und Bekämpfung der Problematik. In diesem Zusammenhang kristallisierte sich ein pragmatischer Ansatz heraus. "[B]esonders häufig auftretende terroristische Aktivitäten [wurden] zum Gegenstand spezifischer Konventionen gemacht" (Finke/Wandscher 2001, 169).Nahezu alle von der Generalversammlung und den Sonderorganisationen verabschiedeten Abkommen können aufgrund bestimmter Kernelemente als Antiterrorkonventionen bezeichnet werden. Zu den besagten Kernelementen gehört zunächst einmal die Verpflichtung der Vertragsstaaten, die in dem jeweiligen Abkommen genannte strafbare Handlung in das jeweilige innerstaatliche Recht aufzunehmen und angemessen zu bestrafen.Hinzu kommt, dass verdächtige Personen entweder durch den Staat selbst zu verfolgen sind oder an einen anderen, verfolgungswilligen Staat ausgeliefert werden müssen. Eine Auslieferung kann nur dann verweigert werden, wenn das Auslieferungsgesuch aufgrund religiöser, ethischer, nationaler, rassistischer oder politischer Gründe erfolgt ist. Ferner sind die Vertragsstaaten dazu verpflichtet, untereinander zu kooperieren und sich gegenseitig Rechtshilfe zu gewähren (vgl. Finke/Wandscher 2001, 169).Das erste derartige Übereinkommen stellt das Haager Abkommen von 1970 zur Bekämpfung der widerrechtlichen Inbesitznahme von Luftfahrzeugen dar. Darauf folgte das Montrealer Abkommen von 1971 zur Bekämpfung widerrechtlicher Handlungen gegen die Sicherheit der Zivilluftfahrt (vgl. ebd., 169). Die besagten Abkommen ordnen bestimmten Aktivitäten zwar das Adjektiv terroristisch zu, stufen diese jedoch nicht als Bedrohung des Weltfriedens ein oder führen zu der Anordnung von Zwangsmaßnahmen gemäß Kapitel VII der UN-Charta durch den Sicherheitsrat.Dies änderte sich mit der Explosion einer Bombe an Bord des Pan-American-Flugs 103 über der schottischen Ortschaft Lockerbie im Jahr 1988. Hier wurden zwei Staatsangehörige Libyens für die Anschläge verantwortlich gemacht, und das Land von den Vereinigten Staaten und Großbritannien zu deren Auslieferung aufgefordert. Der libysche Staat verweigerte das. Als Reaktion darauf wurde der Terrorakt im Rahmen der Resolution 731 durch den Sicherheitsrat als Bedrohung des Weltfriedens gemäß Kapitel V Artikel 24 eingestuft.Durch Resolution 748, ebenfalls 1992 verabschiedet, wurde die Nichtauslieferung durch Libyen als "eine Bedrohung des Weltfriedens und der internationalen Sicherheit" (Finke/Wandscher 2001, 171) bezeichnet und Zwangsmaßnahmen gemäß Kapitel VII UN-Charta gegen das Land erlassen (vgl. Behr 2017, 147; Finke/Wandscher 2001, 170f.).Der Einsatz von Zwangsmaßnahmen gemäß Kapitel VII der UN-Charta erwies sich als wirksames Mittel der Terrorismusbekämpfung im Hinblick auf die Durchsetzung bestimmter Maßnahmen. Hierunter fallen insbesonders Maßnahmen, die zwar Gegenstand geltender Antiterrorkonventionen sind, diese durch die betreffenden Staaten jedoch nicht ratifiziert wurden oder die Konvention selbst noch nicht in Kraft getreten ist (vgl. Finke/Wandscher 2001, 171).Diese Strategie des Sicherheitsrates etablierte sich insbesonders hinsichtlich der Situation in Afghanistan. In Folge der Anschläge auf amerikanische Botschaften in Nairobi und Daressalam erließ der Sicherheitsrat mit der Resolution 1267 Individualsanktionen gegen die afghanischen Taliban. Der Grund hierfür war die Tatsache, dass diese den Verantwortlichen für die Anschläge, der Terrorgruppe Al-Qaida und ihrem Anführer Osama bin Laden, Unterstützung gewährte.Insbesonders durch das Einfrieren der finanziellen Mittel, aber auch durch ein Waffenembargo und ein Reiseverbot, sollten diese zur Auslieferung Bin Ladens gezwungen werden. Um die Umsetzung dieser Maßnahmen zu gewährleisten, setzte die Resolution zudem einen Unterausschuss des Sicherheitsrates ein (vgl. Kreuder-Sonnen 2017, 159).Direkte Reaktionen der Staatengemeinschaft auf den 11. September 2001Als erste Reaktion auf die Anschläge des 11. September 2001 wurde vom Sicherheitsrat bereits am Tag nach den Anschlägen die Resolution 1368 erlassen. In dieser wurde der Terrorismus einstimmig als "Bedrohung des Weltfriedens und der internationalen Sicherheit" (UN-Resolution 1368 2001) im Sinne von Art. 39 UN-Charta bezeichnet. Zugleich wurde auf das Recht zur individuellen und zur kollektiven Selbstverteidigung verwiesen (vgl. UN-Resolution 1368 2001).Noch im gleichen Monat, am 28 September 2001, wurde das Recht zur individuellen und kollektiven Selbstverteidigung mit Resolution 1373 bekräftigt und die internationale Staatengemeinschaft aufgefordert, "durch terroristische Handlungen verursachte Bedrohungen […] mit allen Mitteln im Einklang mit der Charta zu bekämpfen" (Resolution 1373 2001).Neben dem Sicherheitsrat der Vereinten Nationen reagierte auch der Nordatlantikrat umgehend. Am 12. September erklärte der damalige Generalsekretär George Robertson die Anschläge zum kollektiven Verteidigungsfall, wodurch Artikel 5 des NATO-Vertrages in Kraft trat. Nach diesem ist jeder Mitgliedstaat verpflichtet, mit von ihm ausgewählten Mitteln zu helfen (vgl. Robertson 2001).Aus amerikanischer Sicht dienten die Anschläge nicht nur dem Zweck der Tötung von amerikanischen Zivilisten, "Bush sah darin die gesamte westliche Zivilisation herausgefordert" (Czempiel 2003, 114). In seiner Rede am 20. September 2001 warnte der amerikanische Präsident alle Staaten hinsichtlich der Unterstützung und der Beherbergung von Terroristen. Innerhalb der Regierung wurde hinsichtlich der Bekämpfungsstrategie "offen von Präemption gesprochen" (Czempiel 2003, 115).Als Adressaten der amerikanischen Drohung kamen insgesamt 60 Länder mit aktiven terroristischen Organisationen in Frage (vgl. ebd., 114). Auch wenn die meisten Attentäter der Anschläge ursprünglich aus Saudi-Arabien stammten, erhärtete sich zunehmend der Verdacht, dass ihre Aktivitäten von Afghanistan aus gelenkt wurden. Im Zuge dessen wurde das Land als "Prototyp" (ebd., 115) für die Terrorismusbekämpfung ausgewählt. Mit der Operation "Enduring Freedom" starteten amerikanische und britische Truppen am 7. Oktober 2001 Angriffe auf Talibanstützpunkte wie etwa auf Regierungsgebäude in Kandahar und Kabul (vgl. Bruha/ Bortfeld 2001, 162; Czempiel 2003, 115).Der Umstand, dass sich am Tag nach den Anschlägen der Sicherheitsrat der Vereinten Nationen mit diesen befasste "ist ein erstaunlicher Beweis für die politische Klugheit der USA" (Tomuschat 2002, 20) hinsichtlich der Legitimation der Reaktion auf diese. In diesem Zusammenhang gilt es sich jedoch zu fragen, ob die genannten Resolutionen das Land tatsächlich zu einem Recht auf Selbstverteidigung gemäß Artikel 51 UN-Charta legitimieren.In Resolution 1368 findet sich in Bezug darauf ein entscheidender Widerspruch, welcher die rechtlich bedeutsamen Aussagen schwer greifbar macht. Dieser bekräftigt das Recht auf individuelle und kollektive Sicherheit im Sinne der Charta, bezeichnet die Angriffe jedoch lediglich als eine Bedrohung des globalen Friedens und der Sicherheit. Die bekundete Entschlossenheit, die Bedrohung "mit allen Mitteln zu bekämpfen" (UN 2001, 315), kann nicht als eine Ermächtigung für einzelne Staaten aufgefasst werden, sondern steht für die grundsätzliche Bereitschaft der internationalen Gemeinschaft.Anders als Resolution 1368 enthält Resolution 1373 mehr rechtlich eindeutige Aussagen. Bereits in der Präambel wird auf die Anwendung der Maßnahmen gemäß Kapitel VII UN-Charta verwiesen. Zudem bestätigt sie die Zulässigkeit des Einsatzes "aller Mittel" durch die Opfer von terroristischen Anschlägen (vgl. UN 2001, 316f.). Es zeigt sich also, dass eine Berechtigung zu der Ausübung des Selbstverteidigungsrechts gemäß Art. 51 UN-Charta durch die Vereinigten Staaten im Rahmen der genannten Resolution durchaus vorliegt (vgl. Tomuschat 2002, 20f.).Nun stellt sich die Frage, ob die Verbindungen zwischen den Anschlägen und dem Taliban-Regime derart offensichtlich waren, dass die militärischen Aktionen gegen die Taliban in Afghanistan unter die Ausübung des Selbstverteidigungsrechts fallen. In diesem Zusammenhang kann man sich nicht auf die genannten Resolutionen berufen, da diese nicht aufzeigen, "gegen wen Gegenwehr zulässig sein soll" (Tomuschat 2002, 21). Folglich gilt es, die Reaktionen des Sicherheitsrates und der Generalversammlung näher zu betrachten.Es zeigt sich, dass beide Institutionen die amerikanisch-britische Militärintervention nicht verurteilten. Vielmehr verabschiedete der Sicherheitsrat am 12. November 2001 einstimmig Resolution 1377. In dieser wurde der Terrorismus als "eine der schwerwiegendsten Bedrohungen des Weltfriedens und der internationalen Sicherheit im 21. Jahrhundert" (UN-Resolution 1377 2001) bezeichnet. Mit dieser Qualifikation wurde implizit der Einsatz von äußersten Mitteln gestattet, da die Resolution keine "Grenzen und Schranken von Gegenmaßnahmen enthält" (Tomuschat 2002, 21). Letztendlich kann man also davon ausgehen, dass die Vereinten Nationen die Ausübung des Selbstverteidigungsrechts gemäß Art. 51 UN-Charta durch die USA als Reaktion auf die Anschläge vom 11. September 2001 zumindest implizit gebilligt haben (vgl. Tomuschat 2002, 21f.).Als Reaktion auf die Anschläge wurden die bislang geltenden Individualsanktionen gegen die afghanischen Taliban und das Terrornetzwerk Al-Qaida mithilfe der Resolution 1390 zu allgemeinen, dauerhaft geltenden Maßnahmen gegen den transnationalen Terrorismus umgewandelt. Damit wurde nicht nur der Adressatenkreis erweitert, es wurde zusätzlich auch die räumliche und die zeitliche Begrenzung aufgehoben.Jede Person, die von einem Staat als Terrorverdächtiger genannt wurde, bekam ab diesem Zeitpunkt die Sanktionen im Hinblick auf das Privatleben, das private Eigentum, auf den Sozialstatus und das Unterhalten von geschäftlichen Beziehungen zu spüren. Fundierte Beweise für eine Aufnahme in die sogenannte "Schwarze Liste" (Kreuder-Sonnen 2017, 160) durch die Staaten waren ebenso wenig notwendig wie eine Begründung gegenüber dem Individuum (vgl. Kreuder- Sonnen 2017, 160).Folgen für die SicherheitspolitikAngesichts der aufgezeigten Gegenmaßnahmen als direkte Reaktion auf die Anschlage des 11. Septembers 2001 wird deutlich, dass man "bezüglich der Reaktion auf den Terrorismus von einer neuen Ära" (Waldmann 2005, 229) ausgehen muss. Es zeigt sich, dass sowohl bei diesen Anschlägen als auch bei terroristischen Anschlägen in den Folgejahren "die durchschnittliche Zahl der Opfer pro Anschlag […] kontinuierlich ansteigt" (Waldmann 2005. 16).Infolgedessen spricht auch Waldmann im Kontext von terroristischen Anschlägen von Kriegshandlungen. Seiner Ansicht nach hat das zunehmende Ausmaß der Anschläge dazu geführt, dass diese nicht mehr als `low intensity´ war, sondern vielmehr als `high intensitiy´ war eingestuft werden müssen. Der Grund hierfür ist seiner Ansicht nach die Tatsache, dass der Begriff des low intensity war neben dem fehlenden Einsatz von konventionellem Kriegsgerät und größeren Truppenverbänden auch einen begrenzten Personen- und Sachschaden impliziert (vgl. Waldmann 2005, 16f.).Auf der internationalen Ebene spiegelten sich die Reaktionen auf das zunehmende Ausmaß der Anschläge vor allem in den zahlreich erlassenen Konventionen und Resolutionen wieder. Hinzu kommt die Tatsache, dass terroristische Anschläge erstmals zu militärischen Interventionen in Länder geführt haben, die sich in erheblicher Entfernung von dem betroffenen Land befinden. Zumindest im Fall von der militärischen Intervention in Afghanistan herrschte eine seltene Einigkeit zwischen den Großmächten im Sicherheitsrat.Ferner führten die Ereignisse zu einem erheblichen Medieninteresse (vgl. Waldmann 2005, 229). Anhand dessen lässt sich "[d]ie neue Einschätzung des gewaltigen, vor allem dem internationalen Terrorismus zugeschriebenen Drohpotentials" (ebd., 230) feststellen. Diese führte zu drei als signifikant zu bezeichnenden Veränderungen im Hinblick auf die Politik und die Einstellung in Bezug auf den Terrorismus (vgl. ebd., 230).Zunächst einmal bewirkte der transnationale Terrorismus in den westlichen Nationen nicht nur einen "politischen Rechtsruck" (ebd., 230) aller regierenden Parteien. Er wirkte sich auch auf alle Ebenen der Gesellschaft aus. Dieser Wandel auf der nationalen Ebene wirkte sich auch auf die Entscheidungen internationaler Gremien aus. Die bislang vorhandene Balance zwischen der individuellen und kollektiven Sicherheit auf der einen Seite und den Grund- und Freiheitsrechten auf der anderen Seite hat sich zunehmend zugunsten des Sicherheitsaspektes verschoben (vgl. ebd., 230).Insbesonders um den Informationsaustausch zwischen den Staaten gewährleisten zu können und damit ein gemeinsames Vorgehen gegen die Bedrohung zu ermöglichen, wurden internationale Instanzen zur Koordinierung geschaffen (vgl. Behr 2017, 151; Waldmann 2005, 231). Ferner erfolgte eine erhöhte Aufmerksamkeit und Ressourcenbereitstellung für national und international agierende Behörden hinsichtlich terroristischer Aktivitäten und damit verbunden eine Reihe neuer, zu diesem Zweck erlassener Gesetze.Neben dem Informationsaustausch wurden auch die Möglichkeiten der Polizei und anderer Instanzen erweitert, um Anschläge bereits im Planungs- und Vorbereitungsstadium erkennen und verhindern zu können. Hierzu gehören beispielsweise Einreiseverbote für Mitglieder islamistischer Gruppierungen. Neben den erweiterten präventiven Maßnahmen wurden auch Notfallszenarien entwickelt, die im Fall eines Anschlags in Kraft treten (vgl. Waldmann 2005, 232).Im Hinblick auf die dargestellten Veränderungen stellt sich in einem nächsten Schritt die Frage, inwiefern weitere Maßnahmen aus der Sicht der Vereinten Nationen erforderlich sein könnten. Nach dem Terrorismusexperten Peter Waldmann "wird keine Unterscheidung zwischen Maßnahmen auf der nationalen und der internationalen Ebene getroffen, weil beide längst immer enger ineinander greifen und in die gleiche Richtung zielen" (Waldmann 2005, 239).Als zentrale Handlungsmaxime benennt Waldmann in diesem Zusammenhang die Tatsache, dass die Strategien gegenüber terroristischen Netzwerken beziehungsweise dem Terrorismus im Allgemeinen "klar, konsistent und glaubhaft" (Waldmann 2005, 239) sein sollen. Hinsichtlich des Umgangs mit dem islamistischen Terrorismus besteht die größte Problematik darin, dass westliche Nationen ihre Glaubhaftigkeit bezüglich ihrer Leitlinien teilweise verlieren. Insbesonders den Vereinigten Staaten von Amerika wird vorgeworfen, dass sie ihren Prinzipien der Demokratie, des Grundrechtsschutz und der Rechtsstaatlichkeit zugunsten von politischen und wirtschaftlichen Interessen teilweise nicht treu sind (vgl. ebd., 240)."Dass sie aus machtpolitischen Erwägungen jederzeit dazu bereit sind, mit Diktaturen Bündnisse zu schließen, und hinter ihrem quasi messianischen Diskurs, es gelte in der ganzen Welt demokratische Verhältnisse herzustellen, nun allzu deutlich das dringende Bestreben durchscheint, der eigenen Wirtschaft lukrative neue Erdölfelder zu erschließen." (Waldmann 2005, 240).Hinsichtlich der Maßnahmen auf der internationalen Ebene gilt es zunächst auf die Transnationalität näher einzugehen. Wie bereits erwähnt, handelt es sich bei terroristischen Gruppen in den meisten Fällen nicht um eine Gruppe aus einem Land, sondern um Angehörige unterschiedlicher Länder, die sich länderübergreifend miteinander vernetzt haben. Um dem begegnen zu können, erscheint es unabdingbar, dass auch Staaten grenzübergreifend miteinander kooperieren. Dies würde eine erhebliche Bereitschaft der Teilnehmenden zu einem Teilverzicht auf ihre staatlichen Souveränitätsräume und ihrer Souveränitätsrechte bedeuten.Hinsichtlich der nationalen und internationalen Rechtsordnungen im Allgemeinen verlangen transnationale Rechtsverstöße auch eine entsprechende Weiterentwicklung des Rechts auf internationaler Ebene. Transnationale Verbrechen können nicht durch an nationale Grenzen gebundenes Recht bekämpft werden, da aufgrund der unterschiedlichen Verfassungen rechtsfreie Sphären auf globaler Ebene entstehen. Folglich ist eine Ausweitung des transnationalen Rechts erforderlich. Hierfür müsste das Völkerrecht, bislang mit dem Staat als Rechtsperson und einer rechtlichen Bindung auf dem staatlichen Territorium, entterritorialisiert werden (vgl. Behr 2017, 151; Schmalenbach 2004, 266).Neben der Kooperation von Staaten und der Erweiterung des internationalen Rechts spricht Ernst-Otto Czempiel von einer "dreigeteilte[n] Strategie" (Czempiel 2003, 57) hinsichtlich der Verhinderung weiterer terroristischer Anschläge. Kurzfristig ist es die Aufgabe der Staaten, weitere Anschläge zu verhindern. In diesem Zusammenhang offenbart sich jedoch eine in demokratischen Staaten schwierige Güterabwägung hinsichtlich des Schutzes der kollektiven Sicherheit und der individuellen Freiheitsrechte (vgl. Czempiel 2003, 57).Die bürgerliche Freiheit stellt in demokratischen Staaten ein hohes Gut dar. Auf der anderen Seite würde der fortschreitende Ausbau des staatlichen Sicherheitsapparates eine "allmähliche Aushöhlung der individuellen Grund- und Freiheitsrechte um des Schutzes angeblich höherwertiger Güter willen" (Waldmann 2005, 242) bedeuten. Die Folge wäre eine Entwicklung des Rechtsstaates hin zu einem "präventiven Sicherheitsstaat" (Waldmann 2005, 242) mit einer teilweisen Abkehr von demokratischen Grundsätzen (vgl. Hofmann 2006, 446; Waldmann 2005, 242).Infolgedessen gilt es mittelfristig, sich mit dem Hintergrund der Akteure auseinanderzusetzen. "Als besonders fruchtbare Brutstätte gelten die zahlreichen `failing states´, also die gescheiterten oder zerfallenen Staaten" (Czempiel 2003, 58). Am Beispiel Afghanistans wird deutlich, dass der Westen einen erheblichen Anteil an dem Scheitern des Landes und an der Entstehung der dort ansässigen Terrorgruppe hatte.Im Zuge des Konflikts mit der Sowjetunion hatte Amerika die Kämpfer unterstützt. Mit dem sowjetischen Abzug endete auch die amerikanische Unterstützung, und das zerstörte Land wurde ebenso wie die von Amerika ausgebildeten Kämpfer sich selbst überlassen. Es gründete sich die Terrorgruppe Al Qaida mit dem neuen Feind in Gestalt der USA. Die Entwicklungen in Afghanistan haben gezeigt, dass bei jeder Einmischung von außen neben den kurzfristigen auch die langfristigen Konsequenzen zu bedenken sind und dass "das Objekt der Einmischung auch politisch und wirtschaftlich davon profitiert" (Czempiel 2003, 58).Aus langfristiger Sicht gilt es, die "Quellen des Terrorismus auszutrocknen" (ebd., 58) und eine Veränderung des Kontextes zu erwirken. In diesem Zusammenhang ist die Stabilisierung der "failing states" von entscheidender Bedeutung. Czempiel spricht von einer Neuordnung der Welt, "die immer mehr als ein Quasi-Binnenraum begriffen und mit entsprechender Strategie bearbeitet werden muss" (ebd., 59). Neben der Verringerung der Dominanz des Westens ist eine Änderung der Werteverteilung und ein Lösen der großen Konflikte erforderlich (vgl. ebd., 59).FazitDie Anschläge in den Vereinigten Staaten von Amerika am 11. September 2001 wirkten sich nicht nur traumatisch auf das "Selbst- und Machtbewusstsein der USA" (Czempiel 2003, 40) aus, sie versetzten auch den Rest der Welt in "Angst und Schrecken" (Czempiel 2003, 40). Zu Beginn des 21. Jahrhunderts erschien eine militärische Auseinandersetzung zwischen zwei Staaten unwahrscheinlich. Vielmehr stellte der Terrorismus als eine "neue Bedrohung von innen durch gesellschaftliche Akteure" (ebd., 57) das größte sicherheitspolitische Risiko insbesonders für westliche Industriestaaten dar. (vgl. ebd., 57). "Der Terror soll Angst und Schrecken verbreiten, ein Gefühl allgemeiner Unsicherheit erzeugen und offene Panik auslösen" (Hofmann 2006, 445). Hinzu kommt, dass mit dieser Form der psychologischen Kriegsführung das Vertrauen innerhalb der Gesellschaft in die politische Führung und in den Staat im Allgemeinen zerstört werden soll.Aus historischer Sicht existiert das Phänomen des Terrorismus seit mehr als 2000 Jahren. "Er hat überlebt, weil es ihm gelungen ist, sich immer wieder an die veränderten Bedingungen und Gegenmaßnahmen anzupassen und die verwundbaren Stellen seines Gegners ausfindig zu machen, um sie für seine Zwecke zu nutzen" (Hofmann 2006, 446). Entsprechend muss bei Gegenmaßnahmen "das gesamte Spektrum der verfügbaren Mitteln […], psychologische und physische, diplomatische und militärische, ökonomische und moralische" (ebd., 445) eingesetzt werden.Es gilt nun abschließend eine Antwort auf die Frage zu finden, inwiefern die Anschläge im Herbst 2001 die Sicherheitspolitik der Vereinten Nationen verändert haben. Kurzfristig führten diese zu einer seltenen Einigkeit der ständigen Mitglieder im UN-Sicherheitsrat, was sich in den zahlreichen erlassenen Resolutionen wiederspiegelt. Darunter fällt auch die Tatsache, dass die internationale Gemeinschaft die Militärintervention in Afghanistan nicht verurteilte, sondern vielmehr den Vereinigten Staaten ihr Recht auf Selbstverteidigung gemäß Art. 51 UN-Charta einstimmig zugestand.Es erwies sich jedoch hinsichtlich der internationalen Zusammenarbeit als problematisch, dass keine einheitliche Definition des Begriffs Terrorismus besteht. Das könnte dazu führen, dass wirtschaftliche Sanktionen oder militärische Aktionen zur Durchsetzung eigener Interessen fälschlicherweise als Terrorismusbekämpfung etikettiert werden.Generell zeigt sich, dass die Anschläge einen erheblichen innenpolitischen Rechtsruck bewirkten, der sich auch auf die Entscheidungen internationaler Gremien auswirkte. Das wurde durch erweiterte Befugnisse für die Polizei und andere Exekutivorgane in Fragen der nationalen und internationalen Sicherheit sichtbar.Mit der Resolution 70/291 stellte der amtierende UN-Generalsekretär Antonio Guterres am 22. Februar 2017 strategische Handlungsoptionen für die Terrorismusbekämpfung vor. Zunächst einmal soll die Effizienz der Vereinten Nationen im Bereich der Terrorbekämpfung allgemein gestärkt werden. Zudem soll die Qualität der Vereinten Nationen hinsichtlich der Unterstützung der Mitgliedsstaaten bei der Umsetzung der UN-Terrorismusbekämpfungsstrategien hinterfragt werden. Hinzu kommt der Anstoß zu einer Debatte hinsichtlich der regionalen und internationalen Zusammenarbeit von Staaten und UN-Sonderorganisationen.Außerdem wurde Wladimir Iwanowitsch Woronkow auf Vorschlag von Guterres zur Umsetzung und Koordinierung der Vorschläge am 21. Juni 2017 als Untergeneralsekretär eingesetzt. Diese strategische Neuausrichtung wird als eine strategische Aufwertung der Terrorismusbekämpfung im Rahmen der Vereinten Nationen verstanden (vgl. Behr 2017, 152).Zusammenfassend zeigt sich also, dass sich die internationale Gemeinschaft der Tatsache bewusst ist, dass eine gemeinsame Strategie zur Bekämpfung des transnationalen Phänomens erforderlich ist. "Wenn wir den Terrorismus erfolgreich bekämpfen wollen, müssen wir ebenso unermüdlich, innovativ und dynamisch vorgehen wie unsere Gegner" (Hoffmann 2006, 446).LiteraturBehr, H. (2017): Die Antiterrorismuspolitik der UN seit dem Jahr 2001. In: Deutsche Gesellschaft für die Vereinten Nationen e.V. [Hrsg.]: Terrorismusbekämpfung und die Vereinten Nationen. S. 147-151.Böhm, A. (2021): Die Gesetzte des Dschungels. In: ZEIT Geschichte 4/21. S 92-97.Czempiel, E.-O. (2003): Weltpolitik im Umbruch. Die Pax Americana, der Terrorismus und die Zukunft der internationalen Beziehungen. München: Verlag C.H.Beck oHG.Finke, J./ Wadscher, C. (2001): Terrorismusbekämpfung jenseits militärischer Gewalt. In: Deutsche Gesellschaft für die Vereinten Nationen e.V. [Hrsg.]: Terrorismusbekämpfung und die Vereinten Nationen. S. 168-173.Geis, A. (2006): Den Krieg überdenken. Kriegsbegriffe und Kriegstheorien in der Kontroverse. Zugriff am 09.03.2022 unter https://www.pw.ovgu.de/ipw_media/Downloads/Geis/Geis__Einleitung_Den_Krieg_berdenken_9_43-p-90.pdf.Hofmann, B. (2006): Terrorismus – der unerklärte Krieg. New York: Columbia University Press.Kahl, M. (2011):Die Militärstrategie der USA nach dem 11. September. In: Bundeszentrale für Politische Bildung [Hrsg.]: Aus Politik und Zeitgeschichte 27/2011. S. 19-24.Kaim, M. (2011): Internationale Sicherheitspolitik nach dem 11. September. In: Bundeszentrale für Politische Bildung [Hrsg.]: Aus Politik und Zeitgeschichte 27/2011. S. 3-9.Kreuder-Sonnen, C. (2017): Terrorismusbekämpfung und die Vereinten Nationen. In: Deutsche Gesellschaft für die Vereinten Nationen e.V. [Hrsg.]: Terrorismusbekämpfung und die Vereinten Nationen. S. 159-163.Pfahl-Traughber, A. (2016): Terrorismus – Merkmale, Formen und Abgrenzungsprobleme. In: Bundeszentrale für Politische Bildung [Hrsg]:Aus Politik und Zeitgeschichte 24-25/ 2016. S. 10-19.Nato Press Releases (2001): Statement by the North Atlantic Council. Zugriff am 09.03.2022 unter https://www.nato.int/docu/pr/2001/p01-124e.htmSchmalenbach, K. (2017): Völker- und unionsrechtliche Anstöße zur Entterritorialisierung des Rechts. In: Vereinigung der deutschen Staatsrechtslehrer [Hrsg]: Grenzüberschreitungen. Berlin: DeGruyter. S. 245-272.Steinberg, G. (2015): Transnationaler Terrorismus. Zugriff am 06.03.2022 unter https://www.bpb.de/shop/zeitschriften/izpb/209663/transnationaler-terrorismus/.Tomuschat, C. (2002): Der 11. September 2001 und seine rechtlichen Konsequenzen. Zugriff am 22.02.2022. unter https://www.ssoar.info/ssoar/bitstream/handle/document/26104/ssoar-2002-tomuschat-der_11_september_2001_und.pdf;jsessionid=A9D1D4BAEDCA16B97394171E0769C782?sequence=1.United Nation publication:(2001): Resolution 1373. Zugriff am 02.03.2022 unter https://www.un.org/depts/german/sr/sr_01-02/sr1368.pdf(2001): Resolution 1377. Zugriff am 26.02.2022 unter https://www.un.org/depts/german/sr/sr_01-02/sr1373.pdf(2002): Resolution 1390. Zugriff am 28.02.2022 unter https://www.un.org/Depts/german/sr/sr_01-02/sr1390.pdf.(2004): Resolution 1566. Zugriff am 01.03.2022 unter https://www.un.org/depts/german/sr/sr_04-05/sr1566.pdf.Vasilache, A. (2006): Hobbes, der Terrorismus und die Angst in der Weltpolitik. Zugriff am 06.03.2022 unter https://publishup.uni-potsdam.de/opus4-ubp/frontdoor/deliver/index/docId/899/file/51_fb_vasilache.pdf.Waldmann, P. (2005): Terrorismus. Provokation der Macht. Hamburg: Murmann Verlag GmbH.
Publisher's version (útgefin grein) ; Objective: To explore genetic and lifestyle risk factors of MRI-defined brain infarcts (BI) in large population-based cohorts. Methods We performed meta-analyses of genome-wide association studies (GWAS) and examined associations of vascular risk factors and their genetic risk scores (GRS) with MRI-defined BI and a subset of BI, namely, small subcortical BI (SSBI), in 18 population-based cohorts (n=20,949) from 5 ethnicities (3,726 with BI, 2,021 with SSBI). Top loci were followed up in 7 population-based cohorts (n = 6,862; 1,483 with BI, 630 with SBBI), and we tested associations with related phenotypes including ischemic stroke and pathologically defined BI. Results: The mean prevalence was 17.7% for BI and 10.5% for SSBI, steeply rising after age 65. Two loci showed genome-wide significant association with BI: FBN2, p = 1.77 × 10-8; and LINC00539/ZDHHC20, p = 5.82 × 10-9. Both have been associated with blood pressure (BP)-related phenotypes, but did not replicate in the smaller follow-up sample or show associations with related phenotypes. Age- and sex-adjusted associations with BI and SSBI were observed for BP traits (p value for BI, p[BI] = 9.38 × 10-25; p [SSBI] = 5.23 × 10-14 for hypertension), smoking (p[BI]= 4.4 × 10-10; p [SSBI] = 1.2 × 10 -4), diabetes (p[BI] = 1.7 × 10 -8; p [SSBI] = 2.8 × 10 -3), previous cardiovascular disease (p [BI] = 1.0 × 10-18; p [SSBI] = 2.3 × 10-7), stroke (p [BI] = 3.9 × 10-69; p [SSBI] = 3.2 × 10 -24), and MRI-defined white matter hyperintensity burden (p [BI]=1.43 × 10-157; p [SSBI] = 3.16 × 10-106), but not with body mass index or cholesterol. GRS of BP traits were associated with BI and SSBI (p ≤ 0.0022), without indication of directional pleiotropy. Conclusion: In this multiethnic GWAS meta-analysis, including over 20,000 population-based participants, we identified genetic risk loci for BI requiring validation once additional large datasets become available. High BP, including genetically determined, was the most significant modifiable, causal risk factor for BI. ; CHAP: R01-AG-11101, R01-AG-030146, NIRP-14-302587. SMART: This study was supported by a grant from the Netherlands Organization for Scientific Research–Medical Sciences (project no. 904-65–095). LBC: The authors thank the LBC1936 participants and the members of the LBC1936 research team who collected and collated the phenotypic and genotypic data. The LBC1936 is supported by Age UK (Disconnected Mind Programme grant). The work was undertaken by The University of Edinburgh Centre for Cognitive Ageing and Cognitive Epidemiology, part of the cross-council Lifelong Health and Wellbeing Initiative (MR/K026992/1). The brain imaging was performed in the Brain Research Imaging Centre (https://www.ed.ac.uk/clinical-sciences/edinburgh-imaging), a center in the SINAPSE Collaboration (sinapse.ac.uk) supported by the Scottish Funding Council and Chief Scientist Office. Funding from the UK Biotechnology and Biological Sciences Research Council (BBSRC) and the UK Medical Research Council is acknowledged. Genotyping was supported by a grant from the BBSRC (ref. BB/F019394/1). PROSPER: The PROSPER study was supported by an investigator-initiated grant obtained from Bristol-Myers Squibb. Prof. Dr. J.W. Jukema is an Established Clinical Investigator of the Netherlands Heart Foundation (grant 2001 D 032). Support for genotyping was provided by the seventh framework program of the European commission (grant 223004) and by the Netherlands Genomics Initiative (Netherlands Consortium for Healthy Aging grant 050-060-810). SCES and SiMES: National Medical Research Council Singapore Centre Grant NMRC/CG/013/2013. C.-Y.C. is supported by the National Medical Research Council, Singapore (CSA/033/2012), Singapore Translational Research Award (STaR) 2013. Dr. Kamran Ikram received additional funding from the Singapore Ministry of Health's National Medical Research Council (NMRC/CSA/038/2013). SHIP: SHIP is part of the Community Medicine Research net of the University of Greifswald, Germany, which is funded by the Federal Ministry of Education and Research (grants no. 01ZZ9603, 01ZZ0103, and 01ZZ0403), the Ministry of Cultural Affairs, as well as the Social Ministry of the Federal State of Mecklenburg–West Pomerania, and the network "Greifswald Approach to Individualized Medicine (GANI_MED)" funded by the Federal Ministry of Education and Research (grant 03IS2061A). Genome-wide data have been supported by the Federal Ministry of Education and Research (grant no. 03ZIK012) and a joint grant from Siemens Healthineers, Erlangen, Germany, and the Federal State of Mecklenburg–West Pomerania. Whole-body MRI was supported by a joint grant from Siemens Healthineers, Erlangen, Germany, and the Federal State of Mecklenburg–West Pomerania. The University of Greifswald is a member of the Caché Campus program of the InterSystems GmbH. OATS (Older Australian Twins Study): OATS was supported by an Australian National Health and Medical Research Council (NHRMC)/Australian Research Council (ARC) Strategic Award (ID401162) and by a NHMRC grant (ID1045325). OATS was facilitated via access to the Australian Twin Registry, which is supported by the NHMRC Enabling Grant 310667. The OATS genotyping was partly supported by a Commonwealth Scientific and Industrial Research Organisation Flagship Collaboration Fund Grant. NOMAS: The Northern Manhattan Study is funded by the NIH grant "Stroke Incidence and Risk Factors in a Tri-Ethnic Region" (NINDS R01NS 29993). TASCOG: NHMRC and Heart Foundation. AGES: The study was funded by the National Institute on Aging (NIA) (N01-AG-12100), Hjartavernd (the Icelandic Heart Association), and the Althingi (the Icelandic Parliament), with contributions from the Intramural Research Programs at the NIA, the National Heart, Lung, and Blood Institute (NHLBI), and the National Institute of Neurological Disorders and Stroke (NINDS) (Z01 HL004607-08 CE). ERF: The ERF study as a part of European Special Populations Research Network (EUROSPAN) was supported by European Commission FP6 STRP grant no. 018947 (LSHG-CT-2006-01947) and also received funding from the European Community's Seventh Framework Programme (FP7/2007–2013)/grant agreement HEALTH-F4-2007-201413 by the European Commission under the programme "Quality of Life and Management of the Living Resources" of 5th Framework Programme (no. QLG2-CT-2002-01254). High-throughput analysis of the ERF data was supported by a joint grant from Netherlands Organization for Scientific Research and the Russian Foundation for Basic Research (NWO-RFBR 047.017.043). Exome sequencing analysis in ERF was supported by the ZonMw grant (project 91111025). Najaf Amin is supported by the Netherlands Brain Foundation (project no. F2013[1]-28). ARIC: The Atherosclerosis Risk in Communities study was performed as a collaborative study supported by NHLBI contracts (HHSN268201100005C, HSN268201100006C, HSN268201100007C, HHSN268201100008C, HHSN268201100009C, HHSN268201100010C, HHSN268201100011C, and HHSN268201100012C), R01HL70825, R01HL087641, R01HL59367, and R01HL086694; National Human Genome Research Institute contract U01HG004402; and NIH contract HHSN268200625226C. Infrastructure was partly supported by grant no. UL1RR025005, a component of the NIH and NIH Roadmap for Medical Research. This project was also supported by NIH R01 grant NS087541 to M.F. FHS: This work was supported by the National Heart, Lung and Blood Institute's Framingham Heart Study (contracts no. N01-HC-25195 and no. HHSN268201500001I), and its contract with Affymetrix, Inc. for genotyping services (contract no. N02-HL-6-4278). A portion of this research utilized the Linux Cluster for Genetic Analysis (LinGA-II) funded by the Robert Dawson Evans Endowment of the Department of Medicine at Boston University School of Medicine and Boston Medical Center. This study was also supported by grants from the NIA (R01s AG033040, AG033193, AG054076, AG049607, AG008122, and U01-AG049505) and the NINDS (R01-NS017950, UH2 NS100605). Dr. DeCarli is supported by the Alzheimer's Disease Center (P30 AG 010129). ASPS: The research reported in this article was funded by the Austrian Science Fund (FWF) grant nos. P20545-P05, P13180, and P20545-B05, by the Austrian National Bank Anniversary Fund, P15435, and the Austrian Ministry of Science under the aegis of the EU Joint Programme–Neurodegenerative Disease Research (JPND) (jpnd.eu). LLS: The Leiden Longevity Study has received funding from the European Union's Seventh Framework Programme (FP7/2007–2011) under grant agreement no. 259679. This study was supported by a grant from the Innovation-Oriented Research Program on Genomics (SenterNovem IGE05007), the Centre for Medical Systems Biology, and the Netherlands Consortium for Healthy Ageing (grant 050-060-810), all in the framework of the Netherlands Genomics Initiative, Netherlands Organization for Scientific Research (NWO), UnileverColworth, and by BBMRI-NL, a Research Infrastructure financed by the Dutch government (NWO 184.021.007). CHS: This CHS research was supported by contracts HHSN268201200036C, HHSN268200800007C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, N01HC85086, N01HC15103, and HHSN268200960009C and grants U01HL080295, R01HL087652, R01HL105756, R01HL103612, R01HL120393, R01HL085251, and R01HL130114 from the NHLBI with additional contribution from NINDS. Additional support was provided through R01AG023629 from the NIA. A full list of principal CHS investigators and institutions can be found at CHS-NHLBI.org. The provision of genotyping data was supported in part by the National Center for Advancing Translational Sciences, CTSI grant UL1TR001881, and the National Institute of Diabetes and Digestive and Kidney Disease Diabetes Research Center grant DK063491 to the Southern California Diabetes Endocrinology Research Center. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. Rotterdam Study: The generation and management of GWAS genotype data for the Rotterdam Study is supported by the Netherlands Organisation of Scientific Research (NWO) Investments (no. 175.010.2005.011, 911-03-012). This study is funded by the Research Institute for Diseases in the Elderly (014-93-015; RIDE2), the Netherlands Genomics Initiative (NGI)/NWO project no. 050-060-810. The Rotterdam Study is funded by Erasmus MC Medical Center and Erasmus MC University, Rotterdam, Netherlands Organization for Health Research and Development (ZonMw), the Research Institute for Diseases in the Elderly (RIDE), the Ministry of Education, Culture and Science, the Ministry for Health, Welfare and Sports, the European Commission (DG XII), and the Municipality of Rotterdam. M.A.I. is supported by an NWO Veni grant (916.13.054). The 3-City Study: The 3-City Study is conducted under a partnership agreement among the Institut National de la Santé et de la Recherche Médicale (INSERM), the University of Bordeaux, and Sanofi-Aventis. The Fondation pour la Recherche Médicale funded the preparation and initiation of the study. The 3C Study is also supported by the Caisse Nationale Maladie des Travailleurs Salariés, Direction Générale de la Santé, Mutuelle Générale de l'Education Nationale (MGEN), Institut de la Longévité, Conseils Régionaux of Aquitaine and Bourgogne, Fondation de France, and Ministry of Research–INSERM Programme "Cohortes et collections de données biologiques." C.T. and S.D. have received investigator-initiated research funding from the French National Research Agency (ANR) and from the Fondation Leducq. S.D. is supported by a starting grant from the European Research Council (SEGWAY), a grant from the Joint Programme of Neurodegenerative Disease research (BRIDGET), from the European Union's Horizon 2020 research and innovation programme under grant agreements No 643417 & No 640643, and by the Initiative of Excellence of Bordeaux University. Part of the computations were performed at the Bordeaux Bioinformatics Center (CBiB), University of Bordeaux. This work was supported by the National Foundation for Alzheimer's Disease and Related Disorders, the Institut Pasteur de Lille, the Labex DISTALZ, and the Centre National de Génotypage. ADGC: The Alzheimer Disease Genetics Consortium is supported by NIH. NIH-NIA supported this work through the following grants: ADGC, U01 AG032984, RC2 AG036528; NACC, U01 AG016976; NCRAD, U24 AG021886; NIA LOAD, U24 AG026395, U24 AG026390; Banner Sun Health Research Institute, P30 AG019610; Boston University, P30 AG013846, U01 AG10483, R01 CA129769, R01 MH080295, R01 AG017173, R01 AG025259, R01AG33193; Columbia University, P50 AG008702, R37 AG015473; Duke University, P30 AG028377, AG05128; Emory University, AG025688; Group Health Research Institute, UO1 AG06781, UO1 HG004610; Indiana University, P30 AG10133; Johns Hopkins University, P50 AG005146, R01 AG020688; Massachusetts General Hospital, P50 AG005134; Mayo Clinic, P50 AG016574; Mount Sinai School of Medicine, P50 AG005138, P01 AG002219; New York University, P30 AG08051, MO1RR00096, UL1 RR029893, 5R01AG012101, 5R01AG022374, 5R01AG013616, 1RC2AG036502, 1R01AG035137; Northwestern University, P30 AG013854; Oregon Health & Science University, P30 AG008017, R01 AG026916; Rush University, P30 AG010161, R01 AG019085, R01 AG15819, R01 AG17917, R01 AG30146; TGen, R01 NS059873; University of Alabama at Birmingham, P50 AG016582, UL1RR02777; University of Arizona, R01 AG031581; University of California, Davis, P30 AG010129; University of California, Irvine, P50 AG016573, P50, P50 AG016575, P50 AG016576, P50 AG016577; University of California, Los Angeles, P50 AG016570; University of California, San Diego, P50 AG005131; University of California, San Francisco, P50 AG023501, P01 AG019724; University of Kentucky, P30 AG028383, AG05144; University of Michigan, P50 AG008671; University of Pennsylvania, P30 AG010124; University of Pittsburgh, P50 AG005133, AG030653; University of Southern California, P50 AG005142; University of Texas Southwestern, P30 AG012300; University of Miami, R01 AG027944, AG010491, AG027944, AG021547, AG019757; University of Washington, P50 AG005136; Vanderbilt University, R01 AG019085; and Washington University, P50 AG005681, P01 AG03991. The Kathleen Price Bryan Brain Bank at Duke University Medical Center is funded by NINDS grant NS39764, NIMH MH60451, and by GlaxoSmithKline. Genotyping of the TGEN2 cohort was supported by Kronos Science. The TGen series was also funded by NIA grant AG041232, the Banner Alzheimer's Foundation, The Johnnie B. Byrd Sr. Alzheimer's Institute, the Medical Research Council, and the state of Arizona and also includes samples from the following sites: Newcastle Brain Tissue Resource (funding via the Medical Research Council [MRC], local NHS trusts, and Newcastle University), MRC London Brain Bank for Neurodegenerative Diseases (funding via the Medical Research Council), South West Dementia Brain Bank (funding via numerous sources including the Higher Education Funding Council for England [HEFCE], Alzheimer's Research Trust [ART], BRACE, as well as North Bristol NHS Trust Research and Innovation Department and DeNDRoN), The Netherlands Brain Bank (funding via numerous sources including Stichting MS Research, Brain Net Europe, Hersenstichting Nederland Breinbrekend Werk, International Parkinson Fonds, Internationale Stiching Alzheimer Onderzoek), Institut de Neuropatologia, Servei Anatomia Patologica, and Universitat de Barcelona). ADNI: Funding for ADNI is through the Northern California Institute for Research and Education by grants from Abbott, AstraZeneca AB, Bayer Schering Pharma AG, Bristol-Myers Squibb, Eisai Global Clinical Development, Elan Corporation, Genentech, GE Healthcare, GlaxoSmithKline, Innogenetics, Johnson & Johnson, Eli Lilly and Co., Medpace, Inc., Merck and Co., Inc., Novartis AG, Pfizer Inc, F. Hoffman-La Roche, Schering-Plough, Synarc, Inc., Alzheimer's Association, Alzheimer's Drug Discovery Foundation, the Dana Foundation, and the National Institute of Biomedical Imaging and Bioengineering and NIA grants U01 AG024904, RC2 AG036535, and K01 AG030514. Support was also provided by the Alzheimer's Association (LAF, IIRG-08-89720; MAP-V, IIRG-05-14147) and the US Department of Veterans Affairs Administration, Office of Research and Development, Biomedical Laboratory Research Program. SiGN: Stroke Genetic Network (SiGN) was supported in part by award nos. U01NS069208 and R01NS100178 from NINDS. Genetics of Early-Onset Stroke (GEOS) Study was supported by the NIH Genes, Environment and Health Initiative (GEI) grant U01 HG004436, as part of the GENEVA consortium under GEI, with additional support provided by the Mid-Atlantic Nutrition and Obesity Research Center (P30 DK072488); and the Office of Research and Development, Medical Research Service, and the Baltimore Geriatrics Research, Education, and Clinical Center of the Department of Veterans Affairs. Genotyping services were provided by the Johns Hopkins University Center for Inherited Disease Research (CIDR), which is fully funded through a federal contract from the NIH to Johns Hopkins University (contract no. HHSN268200782096C). Assistance with data cleaning was provided by the GENEVA Coordinating Center (U01 HG 004446; PI Bruce S. Weir). Study recruitment and assembly of datasets were supported by a Cooperative Agreement with the Division of Adult and Community Health, Centers for Disease Control and Prevention, and by grants from NINDS and the NIH Office of Research on Women's Health (R01 NS45012, U01 NS069208-01). METASTROKE: ASGC: Australian population control data were derived from the Hunter Community Study. This research was funded by grants from the Australian National and Medical Health Research Council (NHMRC Project Grant ID: 569257), the Australian National Heart Foundation (NHF Project Grant ID: G 04S 1623), the University of Newcastle, the Gladys M Brawn Fellowship scheme, and the Vincent Fairfax Family Foundation in Australia. E.G.H. was supported by a Fellowship from the NHF and National Stroke Foundation of Australia (ID: 100071). J.M. was supported by an Australian Postgraduate Award. BRAINS: Bio-Repository of DNA in Stroke (BRAINS) is partly funded by a Senior Fellowship from the Department of Health (UK) to P.S., the Henry Smith Charity, and the UK-India Education Research Institutive (UKIERI) from the British Council. GEOS: Genetics of Early Onset Stroke (GEOS) Study, Baltimore, was supported by GEI Grant U01 HG004436, as part of the GENEVA consortium under GEI, with additional support provided by the Mid-Atlantic Nutrition and Obesity Research Center (P30 DK072488), and the Office of Research and Development, Medical Research Service, and the Baltimore Geriatrics Research, Education, and Clinical Center of the Department of Veterans Affairs. Genotyping services were provided by the Johns Hopkins University Center for Inherited Disease Research (CIDR), which is fully funded through a federal contract from the NIH to the Johns Hopkins University (contract no. HHSN268200782096C). Assistance with data cleaning was provided by the GENEVA Coordinating Center (U01 HG 004446; PI Bruce S. Weir). Study recruitment and assembly of datasets were supported by a Cooperative Agreement with the Division of Adult and Community Health, Centers for Disease Control and Prevention, and by grants from NINDS and the NIH Office of Research on Women's Health (R01 NS45012, U01 NS069208-01). HPS: Heart Protection Study (HPS) (ISRCTN48489393) was supported by the UK MRC, British Heart Foundation, Merck and Co. (manufacturers of simvastatin), and Roche Vitamins Ltd. (manufacturers of vitamins). Genotyping was supported by a grant to Oxford University and CNG from Merck and Co. J.C.H. acknowledges support from the British Heart Foundation (FS/14/55/30806). ISGS: Ischemic Stroke Genetics Study (ISGS)/Siblings With Ischemic Stroke Study (SWISS) was supported in part by the Intramural Research Program of the NIA, NIH project Z01 AG-000954-06. ISGS/SWISS used samples and clinical data from the NIH-NINDS Human Genetics Resource Center DNA and Cell Line Repository (ccr.coriell.org/ninds), human subjects protocol nos. 2003-081 and 2004-147. ISGS/SWISS used stroke-free participants from the Baltimore Longitudinal Study of Aging (BLSA) as controls. The inclusion of BLSA samples was supported in part by the Intramural Research Program of the NIA, NIH project Z01 AG-000015-50, human subjects protocol no. 2003-078. The ISGS study was funded by NIH-NINDS Grant R01 NS-42733 (J.F.M.). The SWISS study was funded by NIH-NINDS Grant R01 NS-39987 (J.F.M.). This study used the high-performance computational capabilities of the Biowulf Linux cluster at the NIH (biowulf.nih.gov). MGH-GASROS: MGH Genes Affecting Stroke Risk and Outcome Study (MGH-GASROS) was supported by NINDS (U01 NS069208), the American Heart Association/Bugher Foundation Centers for Stroke Prevention Research 0775010N, the NIH and NHLBI's STAMPEED genomics research program (R01 HL087676), and a grant from the National Center for Research Resources. The Broad Institute Center for Genotyping and Analysis is supported by grant U54 RR020278 from the National Center for Research resources. Milan: Milano–Besta Stroke Register Collection and genotyping of the Milan cases within CEDIR were supported by the Italian Ministry of Health (grant nos.: RC 2007/LR6, RC 2008/LR6; RC 2009/LR8; RC 2010/LR8; GR-2011-02347041), FP6 LSHM-CT-2007-037273 for the PROCARDIS control samples. WTCCC2: Wellcome Trust Case-Control Consortium 2 (WTCCC2) was principally funded by the Wellcome Trust, as part of the Wellcome Trust Case Control Consortium 2 project (085475/B/08/Z and 085475/Z/08/Z and WT084724MA). The Stroke Association provided additional support for collection of some of the St George's, London cases. The Oxford cases were collected as part of the Oxford Vascular Study, which is funded by the MRC, Stroke Association, Dunhill Medical Trust, National Institute of Health Research (NIHR), and the NIHR Biomedical Research Centre, Oxford. The Edinburgh Stroke Study was supported by the Wellcome Trust (clinician scientist award to C.L.M.S.) and the Binks Trust. Sample processing occurred in the Genetics Core Laboratory of the Wellcome Trust Clinical Research Facility, Western General Hospital, Edinburgh. Much of the neuroimaging occurred in the Scottish Funding Council Brain Imaging Research Centre (https://www.ed.ac.uk/clinical-sciences/edinburgh-imaging), Division of Clinical Neurosciences, University of Edinburgh, a core area of the Wellcome Trust Clinical Research Facility, and part of the SINAPSE (Scottish Imaging Network: A Platform for Scientific Excellence) collaboration (sinapse.ac.uk), funded by the Scottish Funding Council and the Chief Scientist Office. Collection of the Munich cases and data analysis was supported by the Vascular Dementia Research Foundation. This project has received funding from the European Union's Horizon 2020 research and innovation programme under grant agreements no. 666881, SVDs@target (to M.D.) and no. 667375, CoSTREAM (to M.D.); the DFG as part of the Munich Cluster for Systems Neurology (EXC 1010 SyNergy) and the CRC 1123 (B3) (to M.D.); the Corona Foundation (to M.D.); the Fondation Leducq (Transatlantic Network of Excellence on the Pathogenesis of Small Vessel Disease of the Brain) (to M.D.); the e:Med program (e:AtheroSysMed) (to M.D.) and the FP7/2007-2103 European Union project CVgenes@target (grant agreement no. Health-F2-2013-601456) (to M.D.). M.F. and A.H. acknowledge support from the BHF Centre of Research Excellence in Oxford and the Wellcome Trust core award (090532/Z/09/Z). VISP: The GWAS component of the Vitamin Intervention for Stroke Prevention (VISP) study was supported by the US National Human Genome Research Institute (NHGRI), grant U01 HG005160 (PI Michèle Sale and Bradford Worrall), as part of the Genomics and Randomized Trials Network (GARNET). Genotyping services were provided by the Johns Hopkins University Center for Inherited Disease Research (CIDR), which is fully funded through a federal contract from the NIH to Johns Hopkins University. Assistance with data cleaning was provided by the GARNET Coordinating Center (U01 HG005157; PI Bruce S. Weir). Study recruitment and collection of datasets for the VISP clinical trial were supported by an investigator-initiated research grant (R01 NS34447; PI James Toole) from the US Public Health Service, NINDS, Bethesda, MD. Control data obtained through the database of genotypes and phenotypes (dbGAP) maintained and supported by the United States National Center for Biotechnology Information, US National Library of Medicine. WHI: Funding support for WHI-GARNET was provided through the NHGRI GARNET (grant no. U01 HG005152). Assistance with phenotype harmonization and genotype cleaning, as well as with general study coordination, was provided by the GARNET Coordinating Center (U01 HG005157). Funding support for genotyping, which was performed at the Broad Institute of MIT and Harvard, was provided by the GEI (U01 HG004424). R.L. is a senior clinical investigator of FWO Flanders. F.W.A. is supported by a Dekker scholarship-Junior Staff Member 2014T001–Netherlands Heart Foundation and UCL Hospitals NIHR Biomedical Research Centre. ; Peer Reviewed
Lean body mass, consisting mostly of skeletal muscle, is important for healthy aging. We performed a genome-wide association study for whole body (20 cohorts of European ancestry with n = 38,292) and appendicular (arms and legs) lean body mass (n = 28,330) measured using dual energy X-ray absorptiometry or bioelectrical impedance analysis, adjusted for sex, age, height, and fat mass. Twenty-one single-nucleotide polymorphisms were significantly associated with lean body mass either genome wide (p < 5 × 10−8) or suggestively genome wide (p < 2.3 × 10−6). Replication in 63,475 (47,227 of European ancestry) individuals from 33 cohorts for whole body lean body mass and in 45,090 (42,360 of European ancestry) subjects from 25 cohorts for appendicular lean body mass was successful for five single-nucleotide polymorphisms in/near HSD17B11, VCAN, ADAMTSL3, IRS1, and FTO for total lean body mass and for three single-nucleotide polymorphisms in/near VCAN, ADAMTSL3, and IRS1 for appendicular lean body mass. Our findings provide new insight into the genetics of lean body mass. ; We acknowledge the essential role of the Cohorts for Heart and Aging Research in Genome Epidemiology (CHARGE) Consortium in development and support of this manuscript. CHARGE members include the Netherland's Rotterdam Study (RS), Framingham Heart Study (FHS), Cardiovascular Health Study (CHS), the NHLBI's Atherosclerosis Risk in Communities (ARIC) Study, and Iceland's Age, Gene/Environment Susceptibility (AGES) Reykjavik Study. Age, Gene/Environment Susceptibility Reykjavik Study (AGES-Reykjavik): has been funded by NIH contract N01-AG-12100, the NIA Intramural Research Program, Hjartavernd (the Icelandic Heart Association), and the Althingi (the Icelandic Parliament). The study is approved by the Icelandic National Bioethics Committee, (VSN: 00-063) and the Data Protection Authority. The researchers are indebted to the participants for their willingness to participate in the study. Old Order Amish (OOA): this work was supported by NIH research grants U01 HL72515, U01 GM074518, R01 HL088119, R01 AR046838, and U01 HL084756. Partial funding was also provided by the Mid-Atlantic Nutrition and Obesity Research Center of Maryland (P30 DK072488).). L.M.Y.-A. was supported by F32AR059469 from NIH/NIAMS. M.F. was supported by American Heart Association grant 10SDG2690004. Cardiovascular Health Study (CHS): This CHS research was supported by NHLBI contracts N01-HC- 85079, N01-HC-85080, N01-HC-85081, N01-HC-85082, N01-HC-85083, N01-HC-85084, N01-HC-85085, N01-HC-85086; N01-HC-35129, N01 HC-15103, N01 HC-55222, N01-HC-75150, N01-HC-45133, N01-HC-85239, and by HHSN268201200036C and NHLBI grants HL080295, HL087652, HL105756, HL103612, HL120393, and HL130114 with additional contribution from NINDS. Additional support was provided through AG-023629, AG-15928, AG-20098, and AG-027058 from the NIA. See also http://www.chs-nhlbi.org/pi.htm. DNA handling and genotyping at Cedars-Sinai Medical Center was supported in part by the National Center for Research Resources, grant UL1RR033176, and is now at the National Center for Advancing Translational Sciences, CTSI grant UL1TR000124; in addition to the National Institute of Diabetes and Digestive and Kidney Disease grant DK063491 to the Southern California Diabetes Endocrinology Research Center. CoLaus: The CoLaus study received financial contributions from GlaxoSmithKline, the Faculty of Biology and Medicine of Lausanne, and the Swiss National Science Foundation (grants 33CSCO-122661, 33CS30-139468, and 33CS30-148401). We thank Vincent Mooser and Gérard Waeber, Co-PIs of the CoLaus study. Special thanks to Yolande Barreau, Mathieu Firmann, Vladimir Mayor, Anne-Lise Bastian, Binasa Ramic, Martine Moranville, Martine Baumer, Marcy Sagette, Jeanne Ecoffey, and Sylvie Mermoud for data collection. Data analysis was supervised by Sven Bergmann and Jacques S. Beckmann. The computations for this paper were performed in part at the Vital-IT Center for high-performance computing of the Swiss Institute of Bioinformatics. deCODE Study: The study was funded by deCODE Genetics, ehf. We thank all the participants of this study, the staff of deCODE Genetics core facilities and recruitment center and the densitometry clinic at the University Hospital for their important contributions to this work. The EPIC Study: The EPIC Obesity study is funded by Cancer Research United Kingdom and the Medical Research Council. I.B. acknowledges support from EU FP6 funding (contract no. LSHM-CT-2003-503041) and by the Wellcome Trust (WT098051). Erasmus Rucphen Family (ERF) Study: The study was supported by grants from The Netherlands Organisation for Scientific Research (NWO), Erasmus MC, the Centre for Medical Systems Biology (CMSB), and the European Community's Seventh Framework Programme (FP7/2007-2013), ENGAGE Consortium, grant agreement HEALTH-F4-2007-201413. We are grateful to all general practitioners for their contributions, to Petra Veraart for her help in genealogy, Jeannette Vergeer for the supervision of the laboratory work and Peter Snijders for his help in data collection. Fenland: The Fenland Study is funded by the Wellcome Trust and the Medical Research Council, as well as by the Support for Science Funding programme and CamStrad. We are grateful to all the volunteers for their time and help, and to the General Practitioners and practice staff for help with recruitment. We thank the Fenland Study co-ordination team and the Field Epidemiology team of the MRC Epidemiology Unit for recruitment and clinical testing. Tuomas O. Kilpeläinen was supported by the Danish Council for Independent Research (DFF—1333-00124 and Sapere Aude program grant DFF—1331-00730B). Framingham Osteoporosis Study (FOS)/Framingham Heart Study (FHS): The study was funded by grants from the US National Institute for Arthritis, Musculoskeletal and Skin Diseases and National Institute on Aging (R01 AR 41398 and U24AG051129; D.P.K. and R01AR057118; D.K. D.K. was also supported by FP7-PEOPLE-2012-Marie Curie Career Integration Grants (CIG)). The Framingham Heart Study of the National Heart, Lung, and Blood Institute of the National Institutes of Health and Boston University School of Medicine were supported by the National Heart, Lung, and Blood Institute's Framingham Heart Study (N01-HC-25195) and its contract with Affymetrix, Inc. for genotyping services (N02-HL-6-4278). Analyses reflect intellectual input and resource development from the Framingham Heart Study investigators participating in the SNP Health Association Resource (SHARe) project. A portion of this research was conducted using the Linux Cluster for Genetic Analysis (LinGA-II) funded by the Robert Dawson Evans Endowment of the Department of Medicine at Boston University School of Medicine and Boston Medical Center. eQTL HOb Study: The study was supported by Genome Quebec, Genome Canada and the Canadian Institutes of Health Research (CIHR). Gothenburg Osteoporosis and Obesity Determinants Study (GOOD): The study was funded by the Swedish Research Council, the Swedish Foundation for Strategic Research, The ALF/LUA research grant in Gothenburg, the Lundberg Foundation, the Emil and Vera Cornell Foundation, the Torsten and Ragnar Söderberg's Foundation, Petrus and Augusta Hedlunds Foundation, the Västra Götaland Foundation, and the Göteborg Medical Society. We would like to thank Dr Tobias A. Knoch, Luc V. de Zeeuw, Anis Abuseiris, and Rob de Graaf as well as their institutions the Erasmus Computing Grid, Rotterdam, The Netherlands, and especially the national German MediGRID and Services@MediGRID part of the German D-Grid, both funded by the German Bundesministerium fuer Forschung und Technology under grants #01 AK 803 A-H and # 01 IG 07015G for access to their grid resources. We also thank Karol Estrada, Department of Internal Medicine, Erasmus MC, Rotterdam, the Netherlands for advice regarding the grid resources. Health Aging and Body Composition Study (Health ABC): This study was funded by the National Institutes of Aging. This research was supported by NIA contracts N01AG62101, N01AG62103, and N01AG62106. The genome-wide association study was funded by NIA grant 1R01AG032098-01A1 to Wake Forest University Health Sciences and genotyping services were provided by the Center for Inherited Disease Research (CIDR). CIDR is fully funded through a federal contract from the National Institutes of Health to The Johns Hopkins University, contract number HHSN268200782096C. Indiana: We thank the individuals who participated in this study, as well as the study coordinators, without whom this work would not have been possible. This work was supported by National Institutes of Health grants R01 AG 041517 and M01 RR-00750. Genotyping services were provided by CIDR. CIDR is fully funded through a federal contract from the National Institutes of Health to The Johns Hopkins University, contract number HHSN268200782096C. This research was supported in part by the Intramural Research Program of the NIH, National Library of Medicine. Kora (KORA F3 and KORA F4): The KORA research platform was initiated and financed by the Helmholtz Center Munich, German Research Center for Environmental Health, which is funded by the German Federal Ministry of Education and Research (BMBF) and by the State of Bavaria. Part of this work was financed by the German National Genome Research Network (NGFN-2 and NGFNPlus: 01GS0823). Our research was supported within the Munich Center of Health Sciences (MC Health) as part of LMUinnovativ. The London Life Sciences Population (LOLIPOP): The study was funded by the British Heart Foundation, Wellcome Trust, the Medical Research Council, and Kidney Research UK. The study also receives support from a National Institute for Health Research (NIHR) programme grant. Rotterdam Study (RSI, RSII & RSIII): The generation and management of GWAS genotype data for the Rotterdam Study (RS I, RS II, RS III) was executed by the Human Genotyping Facility of the Genetic Laboratory of the Department of Internal Medicine, Erasmus MC, Rotterdam, The Netherlands. The GWAS datasets are supported by the Netherlands Organisation of Scientific Research NWO Investments (no. 175.010.2005.011, 911-03-012), the Genetic Laboratory of the Department of Internal Medicine, Erasmus MC, the Research Institute for Diseases in the Elderly (014-93-015; RIDE2), the Netherlands Genomics Initiative (NGI)/Netherlands Organisation for Scientific Research (NWO) Netherlands Consortium for Healthy Aging (NCHA), project no. 050-060-810. We thank Pascal Arp, Mila Jhamai, Marijn Verkerk, Lizbeth Herrera, Marjolein Peters, MSc, and Carolina Medina-Gomez, MSc, for their help in creating the GWAS database, and Karol Estrada, PhD, Yurii Aulchenko, PhD, and Carolina Medina-Gomez, PhD, for the creation and analysis of imputed data. The Rotterdam Study is funded by Erasmus Medical Center and Erasmus University, Rotterdam, Netherlands Organization for the Health Research and Development (ZonMw), the Research Institute for Diseases in the Elderly (RIDE), the Ministry of Education, Culture and Science, the Ministry for Health, Welfare and Sports, the European Commission (DG XII), and the Municipality of Rotterdam. We are grateful to the study participants, the staff from the Rotterdam Study and the participating general practitioners and pharmacists. We thank Dr Karol Estrada, Dr Fernando Rivadeneira, Dr Tobias A. Knoch, Anis Abuseiris, and Rob de Graaf (Erasmus MC Rotterdam, The Netherlands) for their help in creating GRIMP, and we thank BigGRID, MediGRID, and Services@MediGRID/D-Grid (funded by the German Bundesministerium fuer Forschung und Technology; grants 01 AK 803 A-H, 01 IG 07015G) for access to their grid computing resources. Rush Memory and Aging Project (MAP): The Memory and Aging Project was supported by National Institute on Aging grants R01AG17917, R01AG15819, and R01AG24480, the Illinois Department of Public Health, the Rush Clinical Translational Science Consortium, and a gift from Ms Marsha Dowd. TwinsUK (TUK): The study was funded by the Wellcome Trust, Arthritis Research UK, and the Chronic Disease Research Foundation. The study also received support from a National Institute for Health Research (NIHR) comprehensive Biomedical Research Centre award to Guy's & St Thomas' NHS Foundation Trust in partnership with King's College London. We thank the staff and volunteers of the TwinsUK study. The study was also supported by Israel Science Foundation, grant number 994/10. Age, Gene/Environment Susceptibility Reykjavik Study (AGES-Reykjavik) has been funded by NIH contract N01-AG-12100, the NIA Intramural Research Program, Hjartavernd (the Icelandic Heart Association), and the Althingi (the Icelandic Parliament). The study is approved by the Icelandic National Bioethics Committee (VSN: 00-063) and the Data Protection Authority. The researchers are indebted to the participants for their willingness to participate in the study. Berlin Aging Study II (BASE-II) was supported by the German Federal Ministry of Education and Research (BMBF (grants #16SV5536K, #16SV5537, #16SV5538, and #16SV5837; previously #01UW0808)). Additional contributions (e.g., financial, equipment, logistics, personnel) are made from each of the other participating sites, i.e., the Max Planck Institute for Human Development (MPIB), Max Planck Institute for Molecular Genetics (MPIMG), Charite University Medicine, German Institute for Economic Research (DIW), all located in Berlin, Germany, and University of Lübeck in Lübeck, Germany. B-vitamins in the prevention of osteoporotic fractures (B-PROOF): B-PROOF is supported and funded by The Netherlands Organization for Health Research and Development (ZonMw, grant 6130.0031), the Hague; unrestricted grant from NZO (Dutch Dairy Association), Zoetermeer; Orthica, Almere; NCHA (Netherlands Consortium Healthy Ageing) Leiden/Rotterdam; Ministry of Economic Affairs, Agriculture and Innovation (project KB-15-004-003), the Hague; Wageningen University, Wageningen; VU University Medical Center, Amsterdam; Erasmus Medical Center, Rotterdam. All organizations are based in the Netherlands. We thank Dr Tobias A. Knoch, Anis Abuseiris, Karol Estrada, and Rob de Graaf as well as their institutions the Erasmus Grid Office, Erasmus MC Rotterdam, The Netherlands, and especially the national German MediGRID and Services@MediGRID part of the German D-Grid, both funded by the German Bundesministerium fuer Forschung und Technology (grants #01 AK 803 A-H and #01 IG 07015G) for access to their gird resources. Further, we gratefully thank all participants. Calcium Intake Fracture Outcome Study (CAIFOS): This study was funded by Healthway Health Promotion Foundation of Western Australia, Australasian Menopause Society and the Australian National Health and Medical Research Council Project Grants (254627, 303169, and 572604). We are grateful to the participants of the CAIFOS Study. The salary of Dr Lewis is supported by a National Health and Medical Research Council of Australia Career Development Fellowship. Danish Osteoporosis Study (DOPS): The study was supported by Karen Elise Jensen foundation. Family Heart Study (FamHS): The study was supported by NIH grants R01-HL-117078, R01-HL-087700, and R01-HL-088215 from NHLBI; and R01-DK-089256 and R01-DK-075681 from NIDDK. GenMets (Health 2000): S.R. was supported by the Academy of Finland Center of Excellence in Complex Disease Genetics (213506 and 129680), Academy of Finland (251217), the Finnish foundation for Cardiovascular Research and the Sigrid Juselius Foundation. S.M. was supported by grants #136895 and #141005, V.S. by grants #139635 and 129494, and M.P. by grant #269517 from the Academy of Finland and a grant from the Finnish Foundation for Cardiovascular Research. M.P. was supported by the Yrjö Jahnsson Foundation. Helsinki Birth Cohort Study (HBCS): We thank all study participants as well as everybody involved in the HBCS. HBCS has been supported by grants from the Academy of Finland, the Finnish Diabetes Research Society, Samfundet Folkhälsann, Novo Nordisk Foundation, Liv och Hälsa, Finska Läkaresällskapet, Signe and Ane Gyllenberg Foundation, University of Helsinki, European Science Foundation (EUROSTRESS), Ministry of Education, Ahokas Foundation, Emil Aaltonen Foundation, Juho Vainio Foundation, and Wellcome Trust (grant number WT089062). Johnston County Study: The Johnston County Osteoarthritis Project is supported in part by cooperative agreements S043, S1734, and S3486 from the Centers for Disease Control and Prevention/Association of Schools of Public Health; the NIAMS Multipurpose Arthritis and Musculoskeletal Disease Center grant 5-P60-AR30701; and the NIAMS Multidisciplinary Clinical Research Center grant 5 P60 AR49465-03. Genotyping services were provided by Algynomics company. Korean Genome Epidemiology Study (KoGES): Korean Genome Epidemiology Study (KoGES): This work was supported by the Research Program funded by the Korea Centers for Disease Control and Prevention (found 2001-347-6111-221, 2002-347-6111-221, 2009-E71007-00, 2010-E71004-00). Kora F3 and Kora F4: The KORA research platform was initiated and financed by the Helmholtz Center Munich, German Research Center for Environmental Health, which is funded by the German Federal Ministry of Education and Research (BMBF) and by the State of Bavaria. Part of this work was financed by the German National Genome Research Network (NGFN-2 and NGFNPlus: 01GS0823). Our research was supported within the Munich Center of Health Sciences (MC Health) as part of LMUinnovativ. LOLIP-REP-IA610: The study was supported by the Wellcome Trust. We thank the participants and research teams involved in LOLIPOP. LOLIP-REP-IA_I: The study was supported by the British Heart Foundation Grant SP/04/002. LOLIP-REP-IA_P: The study was supported by the British Heart Foundation Grant SP/04/002. METSIM: The study was supported by the Academy of Finland, the Finnish Diabetes Research Foundation, the Finnish Cardiovascular Research Foundation, the Strategic Research Funding from the University of Eastern Finland, Kuopio, and the EVO grant 5263 from the Kuopio University Hospital. MrOS Sweden: Financial support was received from the Swedish Research Council (2006-3832), the Swedish Foundation for Strategic Research, the ALF/LUA research grant in Gothenburg, the Lundberg Foundation, the Torsten and Ragnar Söderberg's Foundation, Petrus and Augusta Hedlunds Foundation, the Västra Götaland Foundation, the Göteborg Medical Society, and the Novo Nordisk foundation. Greta and Johan Kock Foundation, A. Påhlsson Foundation, A. Osterlund Foundation, Malmö University Hospital Research Foundation, Research and Development Council of Region Skåne, Sweden, the Swedish Medical Society. MrOS US: The Osteoporotic Fractures in Men (MrOS) Study is supported by National Institutes of Health funding. The following institutes provide support: the National Institute on Aging (NIA), the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), the National Center for Advancing Translational Sciences (NCATS), and NIH Roadmap for Medical Research under the following grant numbers: U01 AG027810, U01 AG042124, U01 AG042139, U01 AG042140, U01 AG042143, U01 AG042145, U01 AG042168, U01 AR066160, and UL1 TR000128. The National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) provided funding for the MrOS ancillary study "GWAS in MrOS and SOF" under the grant number RC2ARO58973. Osteoporosis Prospective Risk Assessment study (OPRA): This work was supported by grants from the Swedish Research Council (K2009-53X-14691-07-3, K2010-77PK-21362-01-2), FAS (grant 2007-2125), Greta and Johan Kock Foundation, A. Påhlsson Foundation, A. Osterlund Foundation, Malmö University Hospital Research Foundation, Research and Development Council of Region Skåne, Sweden, the Swedish Medical Society. We are thankful to all the women who kindly participated in the study and to the staff at the Clinical and Molecular Osteoporosis Research Unit for helping in recruitment of study individuals. Orkney Complex Disease Study (ORCADES): ORCADES was supported by the Chief Scientist Office of the Scottish Government (CZB/4/276, CZB/4/710), the Royal Society, the MRC Human Genetics Unit, Arthritis Research UK (17539) and the European Union framework program 6 EUROSPAN project (contract no. LSHG-CT-2006-018947). DNA extractions were performed at the Wellcome Trust Clinical Research Facility in Edinburgh. We acknowledge the invaluable contributions of Lorraine Anderson and the research nurses in Orkney, the administrative team in Edinburgh and the people of Orkney. PEAK 25: This work was supported by grants from the Swedish Research Council (K2009-53X-14691-07-3, K2010-77PK-21362-01-2), FAS (grant 2007-2125), Greta and Johan Kock Foundation, A. Påhlsson Foundation, A. Osterlund Foundation, Malmö University Hospital Research Foundation, Research and Development Council of Region Skåne, Sweden, the Swedish Medical Society. We are thankful to all the women who kindly participated in the study and to the staff at the Clinical and Molecular Osteoporosis Research Unit for helping in recruitment of study individuals. Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS): The study was supported by grants from the Swedish research council (projects 2008-2202 and 2005-8214) and ALF/LUA research grants from Uppsala university hospital, Uppsala, Sweden. Relationship between Insulin Sensitivity and Cardiovascular Disease (RISC): The RISC study is supported by European Union Grant QLG1-CT-2001-01252 and AstraZeneca. We thank Merck Research Labs for conducting DNA genotyping on RISC samples.Rotterdam III: Rotterdam Study (RS): See discovery. SHIP and SHIP TREND: This work was supported by SHIP, which is part of the Community Medicine Research Network of the University of Greifswald, Germany, by the Federal Ministry of Education and Research (01ZZ9603, 01ZZ0103, and 01ZZ0403), the Ministry of Cultural Affairs as well as the Social Ministry of the Federal State of Mecklenburg-West Pomerania and the network "Greifswald Approach to Individualized Medicine (GANI_MED)" funded by the Federal Ministry of Education and Research (03IS2061A). Genome-wide data have been supported by the Federal Ministry of Education and Research (03ZIK012) and a joint grant from Siemens Healthcare, Erlangen, Germany, and the Federal State of Mecklenburg-West Pomerania. The University of Greifswald is a member of the "Center of Knowledge Interchange" program of the Siemens. A.G. and the Cache´ Campus program of the InterSystems GmbH. The SHIP authors are grateful to the contribution of Florian Ernst, Anja Wiechert, and Astrid Petersmann in generating the SNP data and to Mario Stanke for the opportunity to use his Server Cluster for SNP Imputation. Data analyses were further supported by the German Research Foundation (DFG Vo 955/10-1) and the Federal Ministry of Nutrition, Agriculture and Consumer's Safety. SOF: The Study of Osteoporotic Fractures (SOF) is supported by National Institutes of Health funding. The National Institute on Aging (NIA) provides support under the following grant numbers: R01 AG005407, R01 AR35582, R01 AR35583, R01 AR35584, R01 AG005394, R01 AG027574, and R01 AG027576. The National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) provided funding for the SOF ancillary study "GWAS in MrOS and SOF" under the grant number RC2ARO58973. Uppsala Longitudinal Study of Adult Men (ULSAM): The study was funded by grants from the Swedish research council (projects 2008-2202 and 2005-8214), the Wallenberg foundation, and ALF/LUA research grants from Uppsala university hospital, Uppsala, Sweden. Andrew P. Morris is a Wellcome Trust Senior Fellow in Basic Biomedical Science, grant number WT098017. CROATIA-VIS (VIS): The CROATIA-Vis study was funded by grants from the Medical Research Council (UK) and Republic of Croatia Ministry of Science, Education and Sports research grants to I.R. (108-1080315-0302). We acknowledge the staff of several institutions in Croatia that supported the field work, including but not limited to The University of Split and Zagreb Medical Schools, the Institute for Anthropological Research in Zagreb and Croatian Institute for Public Health. The SNP genotyping for the CROATIA-Vis cohort was performed in the core genotyping laboratory of the Wellcome Trust Clinical Research Facility at the Western General Hospital, Edinburgh, Scotland. Women's Health Initiative (WHI): The WHI program is funded by the National Heart, Lung, and Blood Institute, National Institutes of Health, US Department of Health and Human Services through contracts N01WH22110, 24152, 32100–2, 32105–6, 32108–9, 32111–13, 32115, 32118–32119, 32122, 42107–26, 42129–32, and 44221. We thank the WHI investigators and staff for their dedication, and the study participants for making the program possible. A listing of WHI investigators can be found at https://www.whi.org/researchers/Documents%20%20Write%20a%20Paper/WHI%20Investigator%20Short%20List.pdf. FUSION: This research was supported in part by US National Institutes of Health grants 1-ZIA-HG000024 (to F.S.C.), U01DK062370 (to M.B.), R00DK099240 (to S.C.J.P.), the American Diabetes Association Pathway to Stop Diabetes Grant 1-14-INI-07 (to S.C.J.P.), and Academy of Finland Grants 271961 and 272741 (to M.L.) and 258753 (to H.A.K.). We thank all the subjects for participation and the study personnel for excellent technical assistance. The Pima Indian Study: This study was supported by the Intramural Research Program of the National Institute of Diabetes and Digestive and Kidney Diseases, NIH, USA. Studies of a Targeted Risk Reduction Intervention with Defined Exercise (STRRIDE): This study was supported by the National Heart Lung and Blood Institute of the National Institutes of Health, HL57453 (WEK). Gene expression in old and young muscle biopsies: S.M. and T.G. were supported in part by NIH U24AG051129. ; Peer Reviewed
Only Vanderbilt University affiliated authors are listed on VUIR. For a full list of authors, access the version of record at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6715680/ ; Fanconi anemia (FA) is a genetically heterogeneous disorder with 22 disease-causing genes reported to date. In some FA genes, monoallelic mutations have been found to be associated with breast cancer risk, while the risk associations of others remain unknown. The gene for FA type C, FANCC, has been proposed as a breast cancer susceptibility gene based on epidemiological and sequencing studies. We used the Oncoarray project to genotype two truncating FANCC variants (p.R185X and p.R548X) in 64,760 breast cancer cases and 49,793 controls of European descent. FANCC mutations were observed in 25 cases (14 with p.R185X, 11 with p.R548X) and 26 controls (18 with p.R185X, 8 with p.R548X). There was no evidence of an association with the risk of breast cancer, neither overall (odds ratio 0.77, 95% CI 0.44-1.33, p = 0.4) nor by histology, hormone receptor status, age or family history. We conclude that the breast cancer risk association of these two FANCC variants, if any, is much smaller than for BRCA1, BRCA2 or PALB2 mutations. If this applies to all truncating variants in FANCC it would suggest there are differences between FA genes in their roles on breast cancer risk and demonstrates the merit of large consortia for clarifying risk associations of rare variants. ; We thank all the individuals who took part in these studies and all the researchers, clinicians, technicians and administrative staff who have enabled this work to be carried out. We acknowledge all contributors to the COGS and OncoArray study design, chip design, genotyping, and genotype analyses. ABCFS thank Maggie Angelakos, Judi Maskiell, Gillian Dite. ABCS thanks the Blood bank Sanquin, The Netherlands. ABCTB Investigators: C.L.C., Rosemary Balleine, Robert Baxter, Stephen Braye, Jane Carpenter, Jane Dahlstrom, John Forbes, Soon Lee, Deborah Marsh, Adrienne Morey, Nirmala Pathmanathan, Rodney Scott, Allan Spigelman, Nicholas Wilcken, Desmond Yip. Samples are made available to researchers on a non-exclusive basis. The ACP study wishes to thank the participants in the Thai Breast Cancer study. Special Thanks also go to the Thai Ministry of Public Health (MOPH), doctors and nurses who helped with the data collection process. Finally, the study would like to thank Dr Prat Boonyawongviroj, the former Permanent Secretary of MOPH and Dr Pornthep Siriwanarungsan, the Department Director-General of Disease Control who have supported the study throughout. BBCS thanks Eileen Williams, Elaine Ryder-Mills, Kara Sargus. BCEES thanks Allyson Thomson, Christobel Saunders, Terry Slevin, BreastScreen Western Australia, Elizabeth Wylie, Rachel Lloyd. The BCINIS study would not have been possible without the contributions of Dr. K. Landsman, Dr. N. Gronich, Dr. A. Flugelman, Dr. W. Saliba, Dr. E. Liani, Dr. I. Cohen, Dr. S. Kalet, Dr. V. Friedman, Dr. O. Barnet of the NICCC in Haifa, and all the contributing family medicine, surgery, pathology and oncology teams in all medical institutes in Northern Israel. The BREOGAN study would not have been possible without the contributions of the following: Jose Esteban Castelao, Angel Carracedo, Victor Munoz Garzon, Alejandro Novo Dominguez, Sara Miranda Ponte, Carmen Redondo Marey, Maite Pena Fernandez, Manuel Enguix Castelo, Maria Torres, Manuel Calaza (BREOGAN), Jose Antunez, Maximo Fraga and the staff of the Department of Pathology and Biobank of the University Hospital Complex of Santiago-CHUS, Instituto de Investigacion Sanitaria de Santiago, IDIS, Xerencia de Xestion Integrada de Santiago-SERGAS; Joaquin Gonzalez-Carrero and the staff of the Department of Pathology and Biobank of University Hospital Complex of Vigo, Instituto de Investigacion Biomedica Galicia Sur, SERGAS, Vigo, Spain. BSUCH thanks Peter Bugert, Medical Faculty Mannheim. The CAMA study would like to recognize CONACyT for the financial support provided for this work and all physicians responsible for the project in the different participating hospitals: Dr. German Castelazo (IMSS, Ciudad de Mexico, DF), Dr. Sinhue Barroso Bravo (IMSS, Ciudad de Mexico, DF), Dr. Fernando Mainero Ratchelous (IMSS, Ciudad de Mexico, DF), Dr. Joaquin Zarco Mendez (ISSSTE, Ciudad de Mexico, DF), Dr. Edelmiro Perez Rodriguez (Hospital Universitario, Monterrey, Nuevo Leon), Dr. Jesus Pablo Esparza Cano (IMSS, Monterrey, Nuevo Leon), Dr. Heriberto Fabela (IMSS, Monterrey, Nuevo Leon), Dr. Fausto Hernandez Morales (ISSSTE, Veracruz, Veracruz), Dr. Pedro Coronel Brizio (CECAN SS, Xalapa, Veracruz) and Dr. Vicente A. Saldana Quiroz (IMSS, Veracruz, Veracruz). CBCS thanks study participants, co-investigators, collaborators and staff of the Canadian Breast Cancer Study, and project coordinators Agnes Lai and Celine Morissette. CCGP thanks Styliani Apostolaki, Anna Margiolaki, Georgios Nintos, Maria Perraki, Georgia Saloustrou, Georgia Sevastaki, Konstantinos Pompodakis. CGPS thanks staff and participants of the Copenhagen General Population Study. For the excellent technical assistance: Dorthe Uldall Andersen, Maria Birna Arnadottir, Anne Bank, Dorthe Kjeldgard Hansen. The Danish Cancer Biobank is acknowledged for providing infrastructure for the collection of blood samples for the cases. COLBCCC thanks all patients, the physicians Justo G. Olaya, Mauricio Tawil, Lilian Torregrosa, Elias Quintero, Sebastian Quintero, Claudia Ramirez, Jose J. Caicedo, and Jose F. Robledo, the researchers Ignacio Briceno, Fabian Gil, Angela Umana, Angela Beltran and Viviana Ariza, and the technician Michael Gilbert for their contributions and commitment to this study. Investigators from the CPSII cohort thank the participants and Study Management Group for their invaluable contributions to this research. They also acknowledge the contribution to this study from central cancer registries supported through the Centers for Disease Control and Prevention National Program of Cancer Registries, as well as cancer registries supported by the National Cancer Institute Surveillance Epidemiology and End Results program. CTS Investigators include Leslie Bernstein, S.L.N., James Lacey, Sophia Wang, and Huiyan Ma at the Beckman Research Institute of City of Hope, Jessica Clague DeHart at the School of Community and Global Health Claremont Graduate University, Dennis Deapen, Rich Pinder, and Eunjung Lee at the University of Southern California, Pam Horn-Ross, Christina Clarke Dur and David Nelson at the Cancer Prevention Institute of California, Peggy Reynolds, at the Department of Epidemiology and Biostatistics, University of California San Francisco, H.A-C, A.Z., and Hannah Park at the University of California Irvine, and Fred Schumacher at Case Western University. DIETCOMPLYF thanks the patients, nurses and clinical staff involved in the study. We thank the participants and the investigators of EPIC (European Prospective Investigation into Cancer and Nutrition). ESTHER thanks Hartwig Ziegler, Sonja Wolf, Volker Hermann, Christa Stegmaier, Katja Butterbach. FHRISK thanks NIHR for funding. GC-HBOC thanks Stefanie Engert, Heide Hellebrand, Sandra Krober and LIFE -Leipzig Research Centre for Civilization Diseases (Markus Loeffler, Joachim Thiery, Matthias Nuchter, Ronny Baber). The GENICA Network: Dr. Margarete Fischer-Bosch-Institute of Clinical Pharmacology, Stuttgart, and University of Tubingen, Germany [H.B., W-Y.L.], German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ) [H. B.], Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany's Excellence Strategy - EXC 2180 -390900677, Department of Internal Medicine, Evangelische Kliniken Bonn gGmbH, Johanniter Krankenhaus, Bonn, Germany [Yon-Dschun Ko, Christian Baisch], Institute of Pathology, University of Bonn, Germany [Hans-Peter Fischer], Molecular Genetics of Breast Cancer, Deutsches Krebsforschungszentrum (DKFZ), Heidelberg, Germany [UH], Institute for Prevention and Occupational Medicine of the German Social Accident Insurance, Institute of the Ruhr University Bochum (IPA), Bochum, Germany [Thomas Bruning, Beate Pesch, Sylvia Rabstein, Anne Lotz]; and Institute of Occupational Medicine and Maritime Medicine, University Medical Center Hamburg-Eppendorf, Germany [Volker Harth]. HABCS thanks Michael Bremer and Johann H. Karstens. HEBCS thanks Sofia Khan, Johanna Kiiski, Kristiina Aittomaki, Rainer Fagerholm, Kirsimari Aaltonen, Karl von Smitten, Irja Erkkila. HKBCS thanks Hong Kong Sanatorium and Hospital, Dr Ellen Li Charitable Foundation, The Kerry Group Kuok Foundation, National Institute of Health 1R03CA130065 and the North California Cancer Center for support. HMBCS thanks Johann H. Karstens. HUBCS thanks Shamil Gantsev. KARMA thanks the Swedish Medical Research Counsel. KBCP thanks Eija Myohanen, Helena Kemilainen. We thank all investigators of the KOHBRA (Korean Hereditary Breast Cancer) Study. LMBC thanks Gilian Peuteman, Thomas Van Brussel, EvyVanderheyden and Kathleen Corthouts. MABCS thanks Milena Jakimovska (RCGEB "Georgi D. Efremov), Emilija Lazarova (University Clinic of Radiotherapy and Oncology), Katerina Kubelka-Sabit, Mitko Karadjozov (Adzibadem-Sistina Hospital), Andrej Arsovski and Liljana Stojanovska (Re-Medika Hospital) for their contributions and commitment to this study. MARIE thanks Petra Seibold, Dieter Flesch-Janys, Judith Heinz, Nadia Obi, Alina Vrieling, Sabine Behrens, Ursula Eilber, Muhabbet Celik, Til Olchers and Stefan Nickels. MBCSG (Milan Breast Cancer Study Group): Bernard Peissel, Jacopo Azzollini, Dario Zimbalatti, Daniela Zaffaroni, Bernardo Bonanni, Mariarosaria Calvello, Davide Bondavalli, Aliana Guerrieri Gonzaga, Monica Marabelli, Irene Feroce, and the personnel of the Cogentech Cancer Genetic Test Laboratory. We thank the coordinators, the research staff and especially the MMHS participants for their continued collaboration on research studies in breast cancer. MSKCC thanks Marina Corines, Lauren Jacobs. MTLGEBCS would like to thank Martine Tranchant (CHU de QuebecUniversite Laval Research Center), Marie-France Valois, Annie Turgeon and Lea Heguy (McGill University Health Center, Royal Victoria Hospital; McGill University) for DNA extraction, sample management and skillful technical assistance. J. S. is Chair holder of the Canada Research Chair in Oncogenetics. MYBRCA thanks study participants and research staff (particularly Patsy Ng, Nurhidayu Hassan, Yoon Sook-Yee, Daphne Lee, Lee Sheau Yee, Phuah Sze Yee and Norhashimah Hassan) for their contributions and commitment to this study. The NBCS Collaborators would like to thank the Oslo Breast Cancer Research Consortium, OSBREAC (breastcancerresearch. no/osbreac/), for providing samples and phenotype data. NBHS and SBCGS thank study participants and research staff for their contributions and commitment to the studies. We would like to thank the participants and staff of the Nurses' Health Study and Nurses' Health Study II for their valuable contributions as well as the following state cancer registries for their help: AL, AZ, AR, CA, CO, CT, DE, FL, GA, ID, IL, IN, IA, KY, LA, ME, MD, MA, MI, NE, NH, NJ, NY, NC, ND, OH, OK, OR, PA, RI, SC, TN, TX, VA, WA, WY. The authors assume full responsibility for analyses and interpretation of these data. OFBCR thanks Teresa Selander, Nayana Weerasooriya. ORIGO thanks E. Krol-Warmerdam, and J. Blom for patient accrual, administering questionnaires, and managing clinical information. The ORIGO survival data were retrieved from the Leiden hospital-based cancer registry system (ONCDOC) with the help of Dr. J. Molenaar. PBCS thanks Louise Brinton, Mark Sherman, Neonila Szeszenia-Dabrowska, Beata Peplonska, Witold Zatonski, Pei Chao, Michael Stagner. The ethical approval for the POSH study is MREC/00/6/69, UKCRN ID: 1137. We thank staff in the Experimental Cancer Medicine Centre (ECMC) supported Faculty of Medicine Tissue Bank and the Faculty of Medicine DNA Banking resource. PREFACE thanks Sonja Oeser and Silke Landrith. PROCAS thanks NIHR for funding. RBCS thanks Petra Bos, Jannet Blom, Ellen Crepin, Elisabeth Huijskens, Anja Kromwijk-Nieuwlaat, Annette Heemskerk, the Erasmus MC Family Cancer Clinic. We thank the SEARCH and EPIC teams. SGBCC thanks the participants and research coordinator Ms Tan Siew Li. SKKDKFZS thanks all study participants, clinicians, family doctors, researchers and technicians for their contributions and commitment to this study. We thank the SUCCESS Study teams in Munich, Duessldorf, Erlangen and Ulm. SZBCS thanks Ewa Putresza. UCIBCS thanks Irene Masunaka. UKBGS thanks Breast Cancer Now and the Institute of Cancer Research for support and funding of the Breakthrough Generations Study, and the study participants, study staff, and the doctors, nurses and other health care providers and health information sources who have contributed to the study. We acknowledge NHS funding to the Royal Marsden/ICR NIHR Biomedical Research Centre. BCAC is funded by Cancer Research UK [C1287/A16563, C1287/A10118], the European Union's Horizon 2020 Research and Innovation Programme (grant numbers 634935 and 633784 for BRIDGES and B-CAST respectively), and by the European Community's Seventh Framework Programme under grant agreement number 223175 (Grant Number HEALTH-F2-2009-223175) (COGS). The EU Horizon 2020 Research and Innovation Programme funding source had no role in study design, data collection, data analysis, data interpretation or writing of the report. Genotyping of the OncoArray was funded by the NIH Grant U19 CA148065, and Cancer UK Grant C1287/A16563 and the PERSPECTIVE project supported by the Government of Canada through Genome Canada and the Canadian Institutes of Health Research (grant GPH-129344) and, the Ministere de l'Economie, Science et Innovation du Quebec through Genome Quebec and the PSR-SIIRI-701 grant, and the Quebec Breast Cancer Foundation. Funding for the iCOGS infrastructure came from: the European Community's Seventh Framework Programme under grant agreement No. 223175 (HEALTH-F2-2009-223175) (COGS), Cancer Research UK (C1287/A10118, C1287/A10710, C12292/A11174, C1281/A12014, C5047/A8384, C5047/A15007, C5047/A10692, C8197/A16565), the National Institutes of Health (CA128978) and Post-Cancer GWAS initiative (1U19 CA148537, 1U19 CA148065 and 1U19 CA148112 -the GAME-ON initiative), the Department of Defence (W81XWH-10-1-0341), the Canadian Institutes of Health Research (CIHR) for the CIHR Team in Familial Risks of Breast Cancer, and Komen Foundation for the Cure, the Breast Cancer Research Foundation, and the Ovarian Cancer Research Fund. The DRIVE Consortium was funded by U19 CA148065. The Australian Breast Cancer Family Study (ABCFS), BCFR-NY, BCFR-PA, BCFR-UTAH, the Northern California Breast Cancer Family Registry (NCBCFR) and Ontario Familial Breast Cancer Registry (OFBCR) were supported by grant UM1 CA164920 from the National Cancer Institute (USA). The content of this manuscript does not necessarily reflect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the USA Government or the BCFR. The ABCFS was also supported by the National Health and Medical Research Council of Australia, the New South Wales Cancer Council, the Victorian Health Promotion Foundation (Australia) and the Victorian Breast Cancer Research Consortium. J.L.H. is a National Health and Medical Research Council (NHMRC) Senior Principal Research Fellow. M.C.S. is a NHMRC Senior Research Fellow. The ABCS study was supported by the Dutch Cancer Society [grants NKI 2007-3839; 2009 4363]. The Australian Breast Cancer Tissue Bank (ABCTB) was supported by the National Health and Medical Research Council of Australia, The Cancer Institute NSW and the National Breast Cancer Foundation. C.L.C is a NHMRC Principal Research Fellow. The ACP study is funded by the Breast Cancer Research Trust, UK and KM and AL are supported by the NIHR Manchester Biomedical Research Centre and by the ICEP ("This work was also supported by CRUK [grant number C18281/A19169]"). The AHS study is supported by the intramural research program of the National Institutes of Health, the National Cancer Institute (grant number Z01-CP010119), and the National Institute of Environmental Health Sciences (grant number Z01-ES049030). The work of the BBCC was partly funded by ELAN-Fond of the University Hospital of Erlangen. The BBCS is funded by Cancer Research UK and Breast Cancer Now and acknowledges NHS funding to the NIHR Biomedical Research Centre, and the National Cancer Research Network (NCRN). The BCEES was funded by the National Health and Medical Research Council, Australia and the Cancer Council Western Australia and acknowledges funding from the National Breast Cancer Foundation (J.S.). The BREast Oncology GAlician Network (BREOGAN) is funded by Accion Estrategica de Salud del Instituto de Salud Carlos III FIS PI12/02125/Cofinanciado FEDER; Accion Estrategica de Salud del Instituto de Salud Carlos III FIS Intrasalud (PI13/01136); Programa Grupos Emergentes, Cancer Genetics Unit, Instituto de Investigacion Biomedica Galicia Sur. Xerencia de Xestion Integrada de Vigo-SERGAS, Instituto de Salud Carlos III, Spain; Grant 10CSA012E, Conselleria de Industria Programa Sectorial de Investigacion Aplicada, PEME I+ D e I + D Suma del Plan Gallego de Investigacion, Desarrollo e Innovacion Tecnologica de la Conselleria de Industria de la Xunta de Galicia, Spain; Grant EC11-192. Fomento de la Investigacion Clinica Independiente, Ministerio de Sanidad, Servicios Sociales e Igualdad, Spain; and Grant FEDER-Innterconecta. Ministerio de Economia y Competitividad, Xunta de Galicia, Spain. The BSUCH study was supported by the Dietmar-Hopp Foundation, the Helmholtz Society and the German Cancer Research Center (DKFZ). The CAMA study was funded by Consejo Nacional de Ciencia y Tecnologia (CONACyT) (SALUD-2002-C01-7462). Sample collection and processing was funded in part by grants from the National Cancer Institute (NCI R01CA120120 and K24CA169004). CBCS is funded by the Canadian Cancer Society (grant #313404) and the Canadian Institutes of Health Research. CCGP is supported by funding from the University of Crete. The CECILE study was supported by Fondation de France, Institut National du Cancer (INCa), Ligue Nationale contre le Cancer, Agence Nationale de Securite Sanitaire, de l'Alimentation, de l'Environnement et du Travail (ANSES), Agence Nationale de la Recherche (ANR). The CGPS was supported by the Chief Physician Johan Boserup and Lise Boserup Fund, the Danish Medical Research Council, and Herlev and Gentofte Hospital. COLBCCC is supported by the German Cancer Research Center (DKFZ), Heidelberg, Germany. Diana Torres was in part supported by a postdoctoral fellowship from the Alexander von Humboldt Foundation. The American Cancer Society funds the creation, maintenance, and updating of the CPSII cohort. The CTS was supported by the California Breast Cancer Act of 1993, the California Breast Cancer Research Fund (contract 97-10500) and the National Institutes of Health (R01 CA77398, K05 CA136967, UM1 CA164917, and U01 CA199277). Collection of cancer incidence data was supported by the California Department of Public Health as part of the statewide cancer reporting program mandated by California Health and Safety Code Section 103885. HAC receives support from the Lon V Smith Foundation (LVS39420). The University of Westminster curates the DietCompLyf database funded by the charity Against Breast Cancer (Registered Charity No. 1121258) and the NCRN. The coordination of EPIC is financially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The national cohorts are supported by: Ligue Contre le Cancer, Institut Gustave Roussy, Mutuelle Generale de l'Education Nationale, Institut National de la Sante et de la Recherche Medicale (INSERM) (France); German Cancer Aid, German Cancer Research Center (DKFZ), Federal Ministry of Education and Research (BMBF) (Germany); the Hellenic Health Foundation, the Stavros Niarchos Foundation (Greece); Associazione Italiana per la Ricerca sul Cancro-AIRC-Italy and National Research Council (Italy); Dutch Ministry of Public Health, Welfare and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds, Dutch Prevention Funds, Dutch ZON (Zorg Onderzoek Nederland), World Cancer Research Fund (WCRF), Statistics Netherlands (The Netherlands); Health Research Fund (FIS), PI13/00061 to Granada, PI13/01162 to EPIC-Murcia, Regional Governments of Andalucia, Asturias, Basque Country, Murcia and Navarra, ISCIII RETIC (RD06/0020) (Spain); Cancer Research UK (14136 to EPIC-Norfolk; C570/A16491 and C8221/A19170 to EPIC-Oxford), Medical Research Council (1000143 to EPIC-Norfolk, MR/M012190/1 to EPIC-Oxford) (United Kingdom). The ESTHER study was supported by a grant from the Baden Wurttemberg Ministry of Science, Research and Arts. Additional cases were recruited in the context of the VERDI study, which was supported by a grant from the German Cancer Aid (Deutsche Krebshilfe). FHRISK is funded from NIHR grant PGfAR 0707-10031. DGE is supported by the all Manchester NIHR Biomedical Research Centre (IS-BRC-1215-20007). The GC-HBOC (German Consortium of Hereditary Breast and Ovarian Cancer) is supported by the German Cancer Aid (grant no 110837, coordinator: R.K.S., Cologne). This work was also funded by the European Regional Development Fund and Free State of Saxony, Germany (LIFE - Leipzig Research Centre for Civilization Diseases, project numbers 713-241202, 713-241202, 14505/2470, 14575/2470). The GENICA was funded by the Federal Ministry of Education and Research (BMBF) Germany grants 01KW9975/5, 01KW9976/8, 01KW9977/0 and 01KW0114, the Robert Bosch Foundation, Stuttgart, Deutsches Krebsforschungszentrum (DKFZ), Heidelberg, the Institute for Prevention and Occupational Medicine of the German Social Accident Insurance, Institute of the Ruhr University Bochum (IPA), Bochum, as well as the Department of Internal Medicine, Evangelische Kliniken Bonn gGmbH, Johanniter Krankenhaus, Bonn, Germany. The GEPARSIXTO study was conducted by the German Breast Group GmbH. The GESBC was supported by the Deutsche Krebshilfe e.V. [70492] and the German Cancer Research Center (DKFZ). The HABCS study was supported by the Claudia von Schilling Foundation for Breast Cancer Research, by the Lower Saxonian Cancer Society, by the Friends of Hannover Medical School and by the Rudolf Bartling Foundation. The HEBCS was financially supported by the Helsinki University Central Hospital Research Fund, Academy of Finland (266528), the Finnish Cancer Society, and the Sigrid Juselius Foundation. The HERPACC was supported by MEXT Kakenhi (No. 170150181 and 26253041) from the Ministry of Education, Science, Sports, Culture and Technology of Japan, by a Grant-in-Aid for the Third Term Comprehensive 10-Year Strategy for Cancer Control from Ministry Health, Labour and Welfare of Japan, by Health and Labour Sciences Research Grants for Research on Applying Health Technology from Ministry Health, Labour and Welfare of Japan, by National Cancer Center Research and Development Fund, and "Practical Research for Innovative Cancer Control (15ck0106177h0001)" from Japan Agency for Medical Research and development, AMED, and Cancer Bio Bank Aichi. The HMBCS and HUBCS were funded by the German Research Foundation (Do761/10-1) and by the Rudolf Bartling Foundation. The HUBCS was further supported by a grant from the German Federal Ministry of Research and Education (RUS08/017), and by the Russian Foundation for Basic Research and the Federal Agency for Scientific Organizations for support the Bioresource collections and RFBR grants 14-04-97088, 17-29-06014 and 17-44-020498. Financial support for KARBAC was provided through the regional agreement on medical training and clinical research (ALF) between Stockholm County Council and Karolinska Institutet, the Swedish Cancer Society, The Gustav V Jubilee foundation and Bert von Kantzows foundation. The KARMA study was supported by Marit and Hans Rausings Initiative Against Breast Cancer. The KBCP was financially supported by the special Government Funding (EVO) of Kuopio University Hospital grants, Cancer Fund of North Savo, the Finnish Cancer Organizations, and by the strategic funding of the University of Eastern Finland. The KOHBRA study was partially supported by a grant from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), and the National R&D Program for Cancer Control, Ministry of Health & Welfare, Republic of Korea (HI16C1127; 1020350; 1420190). LMBC is supported by the 'Stichting tegen Kanker'. DL is supported by the FWO. The MABCS study is funded by the Research Centre for Genetic Engineering and Biotechnology "Georgi D. Efremov" and supported by the German Academic Exchange Program, DAAD. The MARIE study was supported by the Deutsche Krebshilfe e. V. [70-2892-BR I, 106332, 108253, 108419, 110826, 110828], the Hamburg Cancer Society, the German Cancer Research Center (DKFZ) and the Federal Ministry of Education and Research (BMBF) Germany [01KH0402]. MBCSG is supported by grants from the Italian Association for Cancer Research (AIRC) and by funds from the Italian citizens who allocated the 5/1000 share of their tax payment in support of the Fondazione IRCCS Istituto Nazionale Tumori, according to Italian laws (INT-Institutional strategic projects "5 x 1000"). The MCBCS was supported by the NIH grants CA192393, CA116167, CA176785 an NIH Specialized Program of Research Excellence (SPORE) in Breast Cancer [CA116201], and the Breast Cancer Research Foundation and a generous gift from the David F. and Margaret T. Grohne Family Foundation. MCCS cohort recruitment was funded by VicHealth and Cancer Council Victoria. The MCCS was further supported by Australian NHMRC grants 209057 and 396414, and by infrastructure provided by Cancer Council Victoria. Cases and their vital status were ascertained through the Victorian Cancer Registry (VCR) and the Australian Institute of Health and Welfare (AIHW), including the National Death Index and the Australian Cancer Database. The MEC was supported by NIH grants CA63464, CA54281, CA098758, CA132839 and CA164973. The MISS study is supported by funding from ERC-2011-294576 Advanced grant, Swedish Cancer Society, Swedish Research Council, Local hospital funds, Berta Kamprad Foundation, Gunnar Nilsson. The MMHS study was supported by NIH grants CA97396, CA128931, CA116201, CA140286 and CA177150. MSKCC is supported by grants from the Breast Cancer Research Foundation and Robert and Kate Niehaus Clinical Cancer Genetics Initiative. The work of MTLGEBCS was supported by the Quebec Breast Cancer Foundation, the Canadian Institutes of Health Research for the " CIHR Team in Familial Risks of Breast Cancer" program -grant #CRN-87521 and the Ministry of Economic Development, Innovation and Export Trade - grant #PSR-SIIRI-701. MYBRCA is funded by research grants from the Malaysian Ministry of Higher Education (UM. C/HlR/MOHE/06) and Cancer Research Malaysia. MYMAMMO is supported by research grants from Yayasan Sime Darby LPGA Tournament and Malaysian Ministry of Higher Education (RP046B-15HTM). The NBCS has received funding from the K.G. Jebsen Centre for Breast Cancer Research; the Research Council of Norway grant 193387/V50 (to A-L Borresen-Dale and V.N.K.) and grant 193387/H10 (to A-L Borresen-Dale and V. N. K.), South Eastern Norway Health Authority (grant 39346 to A-L Borresen-Dale) and the Norwegian Cancer Society (to A-L Borresen-Dale and V. N. K.). The NBHS was supported by NIH grant R01CA100374. Biological sample preparation was conducted the Survey and Biospecimen Shared Resource, which is supported by P30 CA68485. The Carolina Breast Cancer Study (NCBCS) was funded by Komen Foundation, the National Cancer Institute (National Cancer Institute CA058223, U54 CA156733, U01 CA179715), and the North Carolina University Cancer Research Fund. The NGOBCS was supported by the National Cancer Center Research and Development Fund. The NHS was supported by NIH grants P01 CA87969, UM1 CA186107, and U19 CA148065. The NHS2 was supported by NIH grants UM1 CA176726 and U19 CA148065. The ORIGO study was supported by the Dutch Cancer Society (RUL 1997-1505) and the Biobanking and Biomolecular Resources Research Infrastructure (BBMRI-NL CP16). The PBCS was funded by Intramural Research Funds of the National Cancer Institute, Department of Health and Human Services, USA. Genotyping for PLCO was supported by the Intramural Research Program of the National Institutes of Health, NCI, Division of Cancer Epidemiology and Genetics. The PLCO is supported by the Intramural Research Program of the Division of Cancer Epidemiology and Genetics and supported by contracts from the Division of Cancer Prevention, National Cancer Institute, National Institutes of Health. The POSH study is funded by Cancer Research UK (grants C1275/A11699, C1275/C22524, C1275/A19187, C1275/A15956 and Breast Cancer Campaign 2010PR62, 2013PR044. PROCAS is funded from NIHR grant PGfAR 0707-10031. The RBCS was funded by the Dutch Cancer Society (DDHK 2004-3124, DDHK 2009-4318). The SASBAC study was supported by funding from the Agency for Science, Technology and Research of Singapore (A*STAR), the US National Institute of Health (NIH) and the Susan G. Komen Breast Cancer Foundation. The SBCGS was supported primarily by NIH grants R01CA64277, R01CA148667, UMCA182910, and R37CA70867. Biological sample preparation was conducted the Survey and Biospecimen Shared Resource, which is supported by P30 CA68485. The scientific development and funding of this project were, in part, supported by the Genetic Associations and Mechanisms in Oncology (GAME-ON) Network U19 CA148065. SEARCH is funded by Cancer Research UK [C490/A10124, C490/A16561] and supported by the UK National Institute for Health Research Biomedical Research Centre at the University of Cambridge. The University of Cambridge has received salary support for PDPP from the NHS in the East of England through the Clinical Academic Reserve. SEBCS was supported by the BRL (Basic Research Laboratory) program through the National Research Foundation of Korea funded by the Ministry of Education, Science and Technology (2012-0000347). SGBCC is funded by the NUS start-up Grant, National University Cancer Institute Singapore (NCIS) Centre Grant and the NMRC Clinician Scientist Award. Additional controls were recruited by the Singapore Consortium of Cohort StudiesMulti-ethnic cohort (SCCS-MEC), which was funded by the Biomedical Research Council, grant number: 05/1/21/19/425. The Sister Study (SISTER) is supported by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences (Z01-ES044005 and Z01-ES049033). The Two Sister Study (2SISTER) was supported by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences (Z01-ES044005 and Z01-ES102245), and, also by a grant from Susan G. Komen for the Cure, grant FAS0703856. SKKDKFZS is supported by the DKFZ. The SMC is funded by the Swedish Cancer Foundation. The SZBCS was supported by Grant PBZ_KBN_122/P05/2004. The TNBCC was supported by: a Specialized Program of Research Excellence (SPORE) in Breast Cancer (CA116201), a grant from the Breast Cancer Research Foundation, a generous gift from the David F. and Margaret T. Grohne Family Foundation and the Ohio State University Comprehensive Cancer Center. The TWBCS is supported by the Taiwan Biobank project of the Institute of Biomedical Sciences, Academia Sinica, Taiwan. The UCIBCS component of this research was supported by the NIH [CA58860, CA92044] and the Lon V Smith Foundation [LVS39420]. The UKBGS is funded by Breast Cancer Now and the Institute of Cancer Research (ICR), London. ICR acknowledges NHS funding to the NIHR Biomedical Research Centre. The UKOPS study was funded by The Eve Appeal (The Oak Foundation) and supported by the National Institute for Health Research University College London Hospitals Biomedical Research Centre. The USRT Study was funded by Intramural Research Funds of the National Cancer Institute, Department of Health and Human Services, USA. The WAABCS study was supported by grants from the National Cancer Institute of the National Institutes of Health (R01 CA89085 and P50 CA125183 and the D43 TW009112 grant), Susan G. Komen (SAC110026), the Dr. Ralph and Marian Falk Medical Research Trust, and the Avon Foundation for Women.
Publisher's version (útgefin grein) ; Breast cancer is a common disease partially caused by genetic risk factors. Germline pathogenic variants in DNA repair genes BRCA1, BRCA2, PALB2, ATM, and CHEK2 are associated with breast cancer risk. FANCM, which encodes for a DNA translocase, has been proposed as a breast cancer predisposition gene, with greater effects for the ER-negative and triple-negative breast cancer (TNBC) subtypes. We tested the three recurrent protein-truncating variants FANCM:p.Arg658*, p.Gln1701*, and p.Arg1931* for association with breast cancer risk in 67,112 cases, 53,766 controls, and 26,662 carriers of pathogenic variants of BRCA1 or BRCA2. These three variants were also studied functionally by measuring survival and chromosome fragility in FANCM−/− patient-derived immortalized fibroblasts treated with diepoxybutane or olaparib. We observed that FANCM:p.Arg658* was associated with increased risk of ER-negative disease and TNBC (OR = 2.44, P = 0.034 and OR = 3.79; P = 0.009, respectively). In a country-restricted analysis, we confirmed the associations detected for FANCM:p.Arg658* and found that also FANCM:p.Arg1931* was associated with ER-negative breast cancer risk (OR = 1.96; P = 0.006). The functional results indicated that all three variants were deleterious affecting cell survival and chromosome stability with FANCM:p.Arg658* causing more severe phenotypes. In conclusion, we confirmed that the two rare FANCM deleterious variants p.Arg658* and p.Arg1931* are risk factors for ER-negative and TNBC subtypes. Overall our data suggest that the effect of truncating variants on breast cancer risk may depend on their position in the gene. Cell sensitivity to olaparib exposure, identifies a possible therapeutic option to treat FANCM-associated tumors. ; Peterlongo laboratory is supported by Associazione Italiana Ricerca sul Cancro (AIRC; IG2015 no.16732) to P. Peterlongo and by a fellowship from Fondazione Umberto Veronesi to G. Figlioli. Surrallés laboratory is supported by the ICREA-Academia program, the Spanish Ministry of Health (projects FANCOSTEM and FANCOLEN), the Spanish Ministry of Economy and Competiveness (projects CB06/07/0023 and RTI2018-098419-B-I00), the European Commission (EUROFANCOLEN project HEALTH-F5-2012-305421 and P-SPHERE COFUND project), the Fanconi Anemia Research Fund Inc, and the "Fondo Europeo de Desarrollo Regional, una manera de hacer Europa" (FEDER). CIBERER is an initiative of the Instituto de Salud Carlos III, Spain. BCAC: we thank all the individuals who took part in these studies and all the researchers, clinicians, technicians and administrative staff who have enabled this work to be carried out. ABCFS thank Maggie Angelakos, Judi Maskiell, Tu Nguyen-Dumont is a National Breast Cancer Foundation (Australia) Career Development Fellow. ABCS thanks the Blood bank Sanquin, The Netherlands. Samples are made available to researchers on a non-exclusive basis. BCEES thanks Allyson Thomson, Christobel Saunders, Terry Slevin, BreastScreen Western Australia, Elizabeth Wylie, Rachel Lloyd. The BCINIS study would not have been possible without the contributions of Dr. Hedy Rennert, Dr. K. Landsman, Dr. N. Gronich, Dr. A. Flugelman, Dr. W. Saliba, Dr. E. Liani, Dr. I. Cohen, Dr. S. Kalet, Dr. V. Friedman, Dr. O. Barnet of the NICCC in Haifa, and all the contributing family medicine, surgery, pathology and oncology teams in all medical institutes in Northern Israel. The BREOGAN study would not have been possible without the contributions of the following: Manuela Gago-Dominguez, Jose Esteban Castelao, Angel Carracedo, Victor Muñoz Garzón, Alejandro Novo Domínguez, Maria Elena Martinez, Sara Miranda Ponte, Carmen Redondo Marey, Maite Peña Fernández, Manuel Enguix Castelo, Maria Torres, Manuel Calaza (BREOGAN), José Antúnez, Máximo Fraga and the staff of the Department of Pathology and Biobank of the University Hospital Complex of Santiago-CHUS, Instituto de Investigación Sanitaria de Santiago, IDIS, Xerencia de Xestion Integrada de Santiago-SERGAS; Joaquín González-Carreró and the staff of the Department of Pathology and Biobank of University Hospital Complex of Vigo, Instituto de Investigacion Biomedica Galicia Sur, SERGAS, Vigo, Spain. BSUCH thanks Peter Bugert, Medical Faculty Mannheim. CBCS thanks study participants, co-investigators, collaborators and staff of the Canadian Breast Cancer Study, and project coordinators Agnes Lai and Celine Morissette. CCGP thanks Styliani Apostolaki, Anna Margiolaki, Georgios Nintos, Maria Perraki, Georgia Saloustrou, Georgia Sevastaki, Konstantinos Pompodakis. CGPS thanks staff and participants of the Copenhagen General Population Study. For the excellent technical assistance: Dorthe Uldall Andersen, Maria Birna Arnadottir, Anne Bank, Dorthe Kjeldgård Hansen. The Danish Cancer Biobank is acknowledged for providing infrastructure for the collection of blood samples for the cases. Investigators from the CPS-II cohort thank the participants and Study Management Group for their invaluable contributions to this research. They also acknowledge the contribution to this study from central cancer registries supported through the Centers for Disease Control and Prevention National Program of Cancer Registries, as well as cancer registries supported by the National Cancer Institute Surveillance Epidemiology and End Results program. The CTS Steering Committee includes Leslie Bernstein, Susan Neuhausen, James Lacey, Sophia Wang, Huiyan Ma, and Jessica Clague DeHart at the Beckman Research Institute of City of Hope, Dennis Deapen, Rich Pinder, and Eunjung Lee at the University of Southern California, Pam Horn-Ross, Peggy Reynolds, Christina Clarke Dur and David Nelson at the Cancer Prevention Institute of California, Hoda Anton-Culver, Argyrios Ziogas, and Hannah Park at the University of California Irvine, and Fred Schumacher at Case Western University. DIETCOMPLYF thanks the patients, nurses and clinical staff involved in the study. The DietCompLyf study was funded by the charity Against Breast Cancer (Registered Charity Number 1121258) and the NCRN. We thank the participants and the investigators of EPIC (European Prospective Investigation into Cancer and Nutrition). ESTHER thanks Hartwig Ziegler, Sonja Wolf, Volker Hermann, Christa Stegmaier, Katja Butterbach. FHRISK thanks NIHR for funding. GC-HBOC thanks Stefanie Engert, Heide Hellebrand, Sandra Kröber and LIFE - Leipzig Research Centre for Civilization Diseases (Markus Loeffler, Joachim Thiery, Matthias Nüchter, Ronny Baber). The GENICA Network: Dr. Margarete Fischer-Bosch-Institute of Clinical Pharmacology, Stuttgart, and University of Tübingen, Germany [HB, Wing-Yee Lo], German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ) [HB], Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany's Excellence Strategy - EXC 2180 - 390900677 [HB], Department of Internal Medicine, Evangelische Kliniken Bonn gGmbH, Johanniter Krankenhaus, Bonn, Germany [Yon-Dschun Ko, Christian Baisch], Institute of Pathology, University of Bonn, Germany [Hans-Peter Fischer], Molecular Genetics of Breast Cancer, Deutsches Krebsforschungszentrum (DKFZ), Heidelberg, Germany [Ute Hamann], Institute for Prevention and Occupational Medicine of the German Social Accident Insurance, Institute of the Ruhr University Bochum (IPA), Bochum, Germany [TB, Beate Pesch, Sylvia Rabstein, Anne Lotz]; and Institute of Occupational Medicine and Maritime Medicine, University Medical Center Hamburg-Eppendorf, Germany [Volker Harth]. HABCS thanks Michael Bremer. HEBCS thanks Heidi Toiminen, Kristiina Aittomäki, Irja Erkkilä and Outi Malkavaara. HMBCS thanks Peter Hillemanns, Hans Christiansen and Johann H. Karstens. HUBCS thanks Shamil Gantsev. KARMA thanks the Swedish Medical Research Counsel. KBCP thanks Eija Myöhänen, Helena Kemiläinen. LMBC thanks Gilian Peuteman, Thomas Van Brussel, EvyVanderheyden and Kathleen Corthouts. MABCS thanks Milena Jakimovska (RCGEB "Georgi D. Efremov), Katerina Kubelka, Mitko Karadjozov (Adzibadem-Sistina" Hospital), Andrej Arsovski and Liljana Stojanovska (Re-Medika" Hospital) for their contributions and commitment to this study. MARIE thanks Petra Seibold, Dieter Flesch-Janys, Judith Heinz, Nadia Obi, Alina Vrieling, Sabine Behrens, Ursula Eilber, Muhabbet Celik, Til Olchers and Stefan Nickels. MBCSG (Milan Breast Cancer Study Group) thanks Daniela Zaffaroni, Irene Feroce, and the personnel of the Cogentech Cancer Genetic Test Laboratory. We thank the coordinators, the research staff and especially the MMHS participants for their continued collaboration on research studies in breast cancer. MSKCC thanks Marina Corines and Lauren Jacobs. MTLGEBCS would like to thank Martine Tranchant (CHU de Québec Research Center), Marie-France Valois, Annie Turgeon and Lea Heguy (McGill University Health Center, Royal Victoria Hospital; McGill University) for DNA extraction, sample management and skillful technical assistance. J.S. is Chairholder of the Canada Research Chair in Oncogenetics. NBHS thanks study participants and research staff for their contributions and commitment to the studies. We would like to thank the participants and staff of the Nurses' Health Study and Nurses' Health Study II for their valuable contributions as well as the following state cancer registries for their help: AL, AZ, AR, CA, CO, CT, DE, FL, GA, ID, IL, IN, IA, KY, LA, ME, MD, MA, MI, NE, NH, NJ, NY, NC, ND, OH, OK, OR, PA, RI, SC, TN, TX, VA, WA, WY. The study protocol was approved by the institutional review boards of the Brigham and Women's Hospital and Harvard T.H. Chan School of Public Health, and those of participating registries as required. The authors assume full responsibility for analyses and interpretation of these data. OFBCR thanks Teresa Selander and Nayana Weerasooriya. ORIGO thanks E. Krol-Warmerdam, and J. Blom for patient accrual, administering questionnaires, and managing clinical information. PBCS thanks Louise Brinton, Mark Sherman, Neonila Szeszenia-Dabrowska, Beata Peplonska, Witold Zatonski, Pei Chao and Michael Stagner. The ethical approval for the POSH study is MREC /00/6/69, UKCRN ID: 1137. We thank staff in the Experimental Cancer Medicine Centre (ECMC) supported Faculty of Medicine Tissue Bank and the Faculty of Medicine DNA Banking resource. PREFACE thanks Sonja Oeser and Silke Landrith. PROCAS thanks NIHR for funding. RBCS thanks Petra Bos, Jannet Blom, Ellen Crepin, Elisabeth Huijskens, Anja Kromwijk-Nieuwlaat, Annette Heemskerk, the Erasmus MC Family Cancer Clinic. We thank the SEARCH and EPIC teams. SKKDKFZS thanks all study participants, clinicians, family doctors, researchers and technicians for their contributions and commitment to this study. We thank the SUCCESS Study teams in Munich, Duessldorf, Erlangen and Ulm. SZBCS thanks Ewa Putresza. UCIBCS thanks Irene Masunaka. UKBGS thanks Breast Cancer Now and the Institute of Cancer Research for support and funding of the Breakthrough Generations Study, and the study participants, study staff, and the doctors, nurses and other health care providers and health information sources who have contributed to the study. We acknowledge NHS funding to the Royal Marsden/ICR NIHR Biomedical Research Centre. CIMBA: we are grateful to all the families and clinicians who contribute to the studies; Sue Healey, in particular taking on the task of mutation classification with the late Olga Sinilnikova; Maggie Angelakos, Judi Maskiell, Helen Tsimiklis; members and participants in the New York site of the Breast Cancer Family Registry; members and participants in the Ontario Familial Breast Cancer Registry; Vilius Rudaitis and Laimonas Griškevičius; Yuan Chun Ding and Linda Steele for their work in participant enrollment and biospecimen and data management; Bent Ejlertsen and Anne-Marie Gerdes for the recruitment and genetic counseling of participants; Alicia Barroso, Rosario Alonso and Guillermo Pita; all the individuals and the researchers who took part in CONSIT TEAM (Consorzio Italiano Tumori Ereditari Alla Mammella), thanks in particular: Giulia Cagnoli, Roberta Villa, Irene Feroce, Mariarosaria Calvello, Riccardo Dolcetti, Giuseppe Giannini, Laura Papi, Gabriele Lorenzo Capone, Liliana Varesco, Viviana Gismondi, Maria Grazia Tibiletti, Daniela Furlan, Antonella Savarese, Aline Martayan, Stefania Tommasi, Brunella Pilato, Isabella Marchi, Elena Bandieri, Antonio Russo, Daniele Calistri and the personnel of the Cogentech Cancer Genetic Test Laboratory, Milan, Italy. FPGMX: members of the Cancer Genetics group (IDIS): Ana Blanco, Miguel Aguado, Uxía Esperón and Belinda Rodríguez. We thank all participants, clinicians, family doctors, researchers, and technicians for their contributions and commitment to the DKFZ study and the collaborating groups in Lahore, Pakistan (Noor Muhammad, Sidra Gull, Seerat Bajwa, Faiz Ali Khan, Humaira Naeemi, Saima Faisal, Asif Loya, Mohammed Aasim Yusuf) and Bogota, Colombia (Diana Torres, Ignacio Briceno, Fabian Gil). Genetic Modifiers of Cancer Risk in BRCA1/2 Mutation Carriers (GEMO) study is a study from the National Cancer Genetics Network UNICANCER Genetic Group, France. We wish to pay a tribute to Olga M. Sinilnikova, who with Dominique Stoppa-Lyonnet initiated and coordinated GEMO until she sadly passed away on the 30th June 2014. The team in Lyon (Olga Sinilnikova, Mélanie Léoné, Laure Barjhoux, Carole Verny-Pierre, Sylvie Mazoyer, Francesca Damiola, Valérie Sornin) managed the GEMO samples until the biological resource centre was transferred to Paris in December 2015 (Noura Mebirouk, Fabienne Lesueur, Dominique Stoppa-Lyonnet). We want to thank all the GEMO collaborating groups for their contribution to this study. Drs.Sofia Khan, Irja Erkkilä and Virpi Palola; The Hereditary Breast and Ovarian Cancer Research Group Netherlands (HEBON) consists of the following Collaborating Centers: Netherlands Cancer Institute (coordinating center), Amsterdam, NL: M.A. Rookus, F.B.L. Hogervorst, F.E. van Leeuwen, M.A. Adank, M.K. Schmidt, N.S. Russell, D.J. Jenner; Erasmus Medical Center, Rotterdam, NL: J.M. Collée, A.M.W. van den Ouweland, M.J. Hooning, C.M. Seynaeve, C.H.M. van Deurzen, I.M. Obdeijn; Leiden University Medical Center, NL: C.J. van Asperen, P. Devilee, T.C.T.E.F. van Cronenburg; Radboud University Nijmegen Medical Center, NL: C.M. Kets, A.R. Mensenkamp; University Medical Center Utrecht, NL: M.G.E.M. Ausems, M.J. Koudijs; Amsterdam Medical Center, NL: C.M. Aalfs, H.E.J. Meijers-Heijboer; VU University Medical Center, Amsterdam, NL: K. van Engelen, J.J.P. Gille; Maastricht University Medical Center, NL: E.B. Gómez-Garcia, M.J. Blok; University of Groningen, NL: J.C. Oosterwijk, A.H. van der Hout, M.J. Mourits, G.H. de Bock; The Netherlands Comprehensive Cancer Organisation (IKNL): S. Siesling, J.Verloop; The nationwide network and registry of histo- and cytopathology in The Netherlands (PALGA): A.W. van den Belt-Dusebout. HEBON thanks the study participants and the registration teams of IKNL and PALGA for part of the data collection. Overbeek; the Hungarian Breast and Ovarian Cancer Study Group members (Janos Papp, Aniko Bozsik, Zoltan Matrai, Miklos Kasler, Judit Franko, Maria Balogh, Gabriella Domokos, Judit Ferenczi, Department of Molecular Genetics, National Institute of Oncology, Budapest, Hungary) and the clinicians and patients for their contributions to this study; HVH (University Hospital Vall d'Hebron) the authors acknowledge the Oncogenetics Group (VHIO) and the High Risk and Cancer Prevention Unit of the University Hospital Vall d'Hebron, Miguel Servet Progam (CP10/00617), and the Cellex Foundation for providing research facilities and equipment; the ICO Hereditary Cancer Program team led by Dr. Gabriel Capella; the ICO Hereditary Cancer Program team led by Dr. Gabriel Capella; Dr Martine Dumont for sample management and skillful assistance; Catarina Santos and Pedro Pinto; members of the Center of Molecular Diagnosis, Oncogenetics Department and Molecular Oncology Research Center of Barretos Cancer Hospital; Heather Thorne, Eveline Niedermayr, all the kConFab investigators, research nurses and staff, the heads and staff of the Family Cancer Clinics, and the Clinical Follow Up Study (which has received funding from the NHMRC, the National Breast Cancer Foundation, Cancer Australia, and the National Institute of Health (USA)) for their contributions to this resource, and the many families who contribute to kConFab; the investigators of the Australia New Zealand NRG Oncology group; members and participants in the Ontario Cancer Genetics Network; Kevin Sweet, Caroline Craven, Julia Cooper, Amber Aielts, and Michelle O'Conor; Christina Selkirk; Helena Jernström, Karin Henriksson, Katja Harbst, Maria Soller, Ulf Kristoffersson; from Gothenburg Sahlgrenska University Hospital: Anna Öfverholm, Margareta Nordling, Per Karlsson, Zakaria Einbeigi; from Stockholm and Karolinska University Hospital: Anna von Wachenfeldt, Annelie Liljegren, Annika Lindblom, Brita Arver, Gisela Barbany Bustinza; from Umeå University Hospital: Beatrice Melin, Christina Edwinsdotter Ardnor, Monica Emanuelsson; from Uppsala University: Hans Ehrencrona, Maritta Hellström Pigg, Richard Rosenquist; from Linköping University Hospital: Marie Stenmark-Askmalm, Sigrun Liedgren; Cecilia Zvocec, Qun Niu; Joyce Seldon and Lorna Kwan; Dr. Robert Nussbaum, Beth Crawford, Kate Loranger, Julie Mak, Nicola Stewart, Robin Lee, Amie Blanco and Peggy Conrad and Salina Chan; Carole Pye, Patricia Harrington and Eva Wozniak. OSUCCG thanks Kevin Sweet, Caroline Craven, Julia Cooper, Michelle O'Conor and Amber Aeilts. BCAC is funded by Cancer Research UK [C1287/A16563, C1287/A10118], the European Union's Horizon 2020 Research and Innovation Programme (grant numbers 634935 and 633784 for BRIDGES and B-CAST respectively), and by the European Community´s Seventh Framework Programme under grant agreement number 223175 (grant number HEALTH-F2-2009-223175) (COGS). The EU Horizon 2020 Research and Innovation Programme funding source had no role in study design, data collection, data analysis, data interpretation or writing of the report. Genotyping of the OncoArray was funded by the NIH Grant U19 CA148065, and Cancer UK Grant C1287/A16563 and the PERSPECTIVE project supported by the Government of Canada through Genome Canada and the Canadian Institutes of Health Research (grant GPH-129344) and, the Ministère de l'Économie, Science et Innovation du Québec through Genome Québec and the PSRSIIRI-701 grant, and the Quebec Breast Cancer Foundation. The Australian Breast Cancer Family Study (ABCFS) was supported by grant UM1 CA164920 from the National Cancer Institute (USA). The content of this manuscript does not necessarily reflect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the USA Government or the BCFR. The ABCFS was also supported by the National Health and Medical Research Council of Australia, the New South Wales Cancer Council, the Victorian Health Promotion Foundation (Australia) and the Victorian Breast Cancer Research Consortium. J.L.H. is a National Health and Medical Research Council (NHMRC) Senior Principal Research Fellow. M.C.S. is a NHMRC Senior Research Fellow. The ABCS study was supported by the Dutch Cancer Society [grants NKI 2007-3839; 2009 4363]. The Australian Breast Cancer Tissue Bank (ABCTB) was supported by the National Health and Medical Research Council of Australia, The Cancer Institute NSW and the National Breast Cancer Foundation. The AHS study is supported by the intramural research program of the National Institutes of Health, the National Cancer Institute (grant number Z01-CP010119), and the National Institute of Environmental Health Sciences (grant number Z01-ES049030). The work of the BBCC was partly funded by ELAN-Fond of the University Hospital of Erlangen. The BBCS is funded by Cancer Research UK and Breast Cancer Now and acknowledges NHS funding to the NIHR Biomedical Research Centre, and the National Cancer Research Network (NCRN). The BCEES was funded by the National Health and Medical Research Council, Australia and the Cancer Council Western Australia. For the BCFR-NY, BCFR-PA, BCFR-UT this work was supported by grant UM1 CA164920 from the National Cancer Institute. The content of this manuscript does not necessarily reflect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government or the BCFR. BCINIS study was funded by the BCRF (The Breast Cancer Research Foundation, USA). The BREast Oncology GAlician Network (BREOGAN) is funded by Acción Estratégica de Salud del Instituto de Salud Carlos III FIS PI12/02125/Cofinanciado FEDER; Acción Estratégica de Salud del Instituto de Salud Carlos III FIS Intrasalud (PI13/01136); Programa Grupos Emergentes, Cancer Genetics Unit, Instituto de Investigacion Biomedica Galicia Sur. Xerencia de Xestion Integrada de Vigo-SERGAS, Instituto de Salud Carlos III, Spain; Grant 10CSA012E, Consellería de Industria Programa Sectorial de Investigación Aplicada, PEME I + D e I + D Suma del Plan Gallego de Investigación, Desarrollo e Innovación Tecnológica de la Consellería de Industria de la Xunta de Galicia, Spain; Grant EC11-192. Fomento de la Investigación Clínica Independiente, Ministerio de Sanidad, Servicios Sociales e Igualdad, Spain; and Grant FEDER-Innterconecta. Ministerio de Economia y Competitividad, Xunta de Galicia, Spain. The BSUCH study was supported by the Dietmar-Hopp Foundation, the Helmholtz Society and the German Cancer Research Center (DKFZ). Sample collection and processing was funded in part by grants from the National Cancer Institute (NCI R01CA120120 and K24CA169004). CBCS is funded by the Canadian Cancer Society (grant # 313404) and the Canadian Institutes of Health Research. CCGP is supported by funding from the University of Crete. The CECILE study was supported by Fondation de France, Institut National du Cancer (INCa), Ligue Nationale contre le Cancer, Agence Nationale de Sécurité Sanitaire, de l'Alimentation, de l'Environnement et du Travail (ANSES), Agence Nationale de la Recherche (ANR). The CGPS was supported by the Chief Physician Johan Boserup and Lise Boserup Fund, the Danish Medical Research Council, and Herlev and Gentofte Hospital. The American Cancer Society funds the creation, maintenance, and updating of the CPS-II cohort. The CTS was initially supported by the California Breast Cancer Act of 1993 and the California Breast Cancer Research Fund (contract 97-10500) and is currently funded through the National Institutes of Health (R01 CA77398, K05 CA136967, UM1 CA164917, and U01 CA199277). Collection of cancer incidence data was supported by the California Department of Public Health as part of the statewide cancer reporting program mandated by California Health and Safety Code Section 103885. The University of Westminster curates the DietCompLyf database funded by Against Breast Cancer Registered Charity No. 1121258 and the NCRN. The coordination of EPIC is financially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The national cohorts are supported by: Ligue Contre le Cancer, Institut Gustave Roussy, Mutuelle Générale de l'Education Nationale, Institut National de la Santé et de la Recherche Médicale (INSERM) (France); German Cancer Aid, German Cancer Research Center (DKFZ), Federal Ministry of Education and Research (BMBF) (Germany); the Hellenic Health Foundation, the Stavros Niarchos Foundation (Greece); Associazione Italiana per la Ricerca sul Cancro-AIRC-Italy and National Research Council (Italy); Dutch Ministry of Public Health, Welfare and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds, Dutch Prevention Funds, Dutch ZON (Zorg Onderzoek Nederland), World Cancer Research Fund (WCRF), Statistics Netherlands (The Netherlands); Health Research Fund (FIS), PI13/00061 to Granada, PI13/01162 to EPIC-Murcia, Regional Governments of Andalucía, Asturias, Basque Country, Murcia and Navarra, ISCIII RETIC (RD06/0020) (Spain); Cancer Research UK (14136 to EPIC-Norfolk; C570/A16491 and C8221/A19170 to EPIC-Oxford), Medical Research Council (1000143 to EPIC-Norfolk, MR/M012190/1 to EPIC-Oxford) (United Kingdom). The ESTHER study was supported by a grant from the Baden Württemberg Ministry of Science, Research and Arts. Additional cases were recruited in the context of the VERDI study, which was supported by a grant from the German Cancer Aid (Deutsche Krebshilfe). FHRISK is funded from NIHR grant PGfAR 0707-10031. The GC-HBOC (German Consortium of Hereditary Breast and Ovarian Cancer) is supported by the German Cancer Aid (grant no 110837, coordinator: Rita K. Schmutzler, Cologne). This work was also funded by the European Regional Development Fund and Free State of Saxony, Germany (LIFE - Leipzig Research Centre for Civilization Diseases, project numbers 713-241202, 713-241202, 14505/2470, 14575/2470). The GENICA was funded by the Federal Ministry of Education and Research (BMBF) Germany grants 01KW9975/5, 01KW9976/8, 01KW9977/0 and 01KW0114, the Robert Bosch Foundation, Stuttgart, Deutsches Krebsforschungszentrum (DKFZ), Heidelberg, the Institute for Prevention and Occupational Medicine of the German Social Accident Insurance, Institute of the Ruhr University Bochum (IPA), Bochum, as well as the Department of Internal Medicine, Evangelische Kliniken Bonn gGmbH, Johanniter Krankenhaus, Bonn, Germany. The GEPARSIXTO study was conducted by the German Breast Group GmbH. The GESBC was supported by the Deutsche Krebshilfe e. V. [70492] and the German Cancer Research Center (DKFZ). The HABCS study was supported by the Claudia von Schilling Foundation for Breast Cancer Research, by the Lower Saxonian Cancer Society, and by the Rudolf Bartling Foundation. The HEBCS was financially supported by the Helsinki University Central Hospital Research Fund, Academy of Finland (266528), the Finnish Cancer Society, and the Sigrid Juselius Foundation. The HMBCS was supported by a grant from the German Research Foundation (Do 761/10-1). The HUBCS was supported by a grant from the German Federal Ministry of Research and Education (RUS08/017), and by the Russian Foundation for Basic Research and the Federal Agency for Scientific Organizations for support the Bioresource collections and RFBR grants 14-04-97088, 17-29-06014 and 17-44-020498. E.K was supported by the program for support the bioresource collections №007-030164/2 and study was performed as part of the assignment of the Ministry of Science and Higher Education of Russian Federation (№АААА-А16-116020350032-1). Financial support for KARBAC was provided through the regional agreement on medical training and clinical research (ALF) between Stockholm County Council and Karolinska Institutet, the Swedish Cancer Society, The Gustav V Jubilee foundation and Bert von Kantzows foundation. The KARMA study was supported by Märit and Hans Rausings Initiative Against Breast Cancer. The KBCP was financially supported by the special Government Funding (EVO) of Kuopio University Hospital grants, Cancer Fund of North Savo, the Finnish Cancer Organizations, and by the strategic funding of the University of Eastern Finland. LMBC is supported by the 'Stichting tegen Kanker'. DL is supported by the FWO. The MABCS study is funded by the Research Centre for Genetic Engineering and Biotechnology "Georgi D. Efremov" and supported by the German Academic Exchange Program, DAAD. The MARIE study was supported by the Deutsche Krebshilfe e.V. [70-2892-BR I, 106332, 108253, 108419, 110826, 110828], the Hamburg Cancer Society, the German Cancer Research Center (DKFZ) and the Federal Ministry of Education and Research (BMBF) Germany [01KH0402]. MBCSG is supported by grants from the Italian Association for Cancer Research (AIRC) and by funds from the Italian citizens who allocated the 5/1000 share of their tax payment in support of the Fondazione IRCCS Istituto Nazionale Tumori, according to Italian laws (INT-Institutional strategic projects "5 × 1000"). The MCBCS was supported by the NIH grants CA192393, CA116167, CA176785 an NIH Specialized Program of Research Excellence (SPORE) in Breast Cancer [CA116201], and the Breast Cancer Research Foundation and a generous gift from the David F. and Margaret T. Grohne Family Foundation. MCCS cohort recruitment was funded by VicHealth and Cancer Council Victoria. The MCCS was further supported by Australian NHMRC grants 209057 and 396414, and by infrastructure provided by Cancer Council Victoria. Cases and their vital status were ascertained through the Victorian Cancer Registry (VCR) and the Australian Institute of Health and Welfare (AIHW), including the National Death Index and the Australian Cancer Database. The MEC was support by NIH grants CA63464, CA54281, CA098758, CA132839 and CA164973. The MISS study is supported by funding from ERC-2011-294576 Advanced grant, Swedish Cancer Society, Swedish Research Council, Local hospital funds, Berta Kamprad Foundation, Gunnar Nilsson. The MMHS study was supported by NIH grants CA97396, CA128931, CA116201, CA140286 and CA177150. MSKCC is supported by grants from the Breast Cancer Research Foundation and Robert and Kate Niehaus Clinical Cancer Genetics Initiative. The work of MTLGEBCS was supported by the Quebec Breast Cancer Foundation, the Canadian Institutes of Health Research for the "CIHR Team in Familial Risks of Breast Cancer" program – grant # CRN-87521 and the Ministry of Economic Development, Innovation and Export Trade – grant # PSR-SIIRI-701. The NBHS was supported by NIH grant R01CA100374. Biological sample preparation was conducted the Survey and Biospecimen Shared Resource, which is supported by P30 CA68485. The Northern California Breast Cancer Family Registry (NC-BCFR) and Ontario Familial Breast Cancer Registry (OFBCR) were supported by grant UM1 CA164920 from the National Cancer Institute (USA). The content of this manuscript does not necessarily reflect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the USA Government or the BCFR. The Carolina Breast Cancer Study was funded by Komen Foundation, the National Cancer Institute (P50 CA058223, U54 CA156733, U01 CA179715), and the North Carolina University Cancer Research Fund. The NHS was supported by NIH grants P01 CA87969, UM1 CA186107, and U19 CA148065. The NHS2 was supported by NIH grants UM1 CA176726 and U19 CA148065. The ORIGO study was supported by the Dutch Cancer Society (RUL 1997-1505) and the Biobanking and Biomolecular Resources Research Infrastructure (BBMRI-NL CP16). The PBCS was funded by Intramural Research Funds of the National Cancer Institute, Department of Health and Human Services, USA. Genotyping for PLCO was supported by the Intramural Research Program of the National Institutes of Health, NCI, Division of Cancer Epidemiology and Genetics. The PLCO is supported by the Intramural Research Program of the Division of Cancer Epidemiology and Genetics and supported by contracts from the Division of Cancer Prevention, National Cancer Institute, National Institutes of Health. The POSH study is funded by Cancer Research UK (grants C1275/A11699, C1275/C22524, C1275/A19187, C1275/A15956 and Breast Cancer Campaign 2010PR62, 2013PR044. PROCAS is funded from NIHR grant PGfAR 0707-10031. The RBCS was funded by the Dutch Cancer Society (DDHK 2004-3124, DDHK 2009-4318). SEARCH is funded by Cancer Research UK [C490/A10124, C490/A16561] and supported by the UK National Institute for Health Research Biomedical Research Centre at the University of Cambridge. The University of Cambridge has received salary support for PDPP from the NHS in the East of England through the Clinical Academic Reserve. The Sister Study (SISTER) is supported by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences (Z01-ES044005 and Z01-ES049033). The Two Sister Study (2SISTER) was supported by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences (Z01-ES044005 and Z01-ES102245), and, also by a grant from Susan G. Komen for the Cure, grant FAS0703856. SKKDKFZS is supported by the DKFZ. The SMC is funded by the Swedish Cancer Foundation and the Swedish Research Council [grant 2017-00644 for the Swedish Infrastructure for Medical Population-based Life-course Environmental Research (SIMPLER)]. The SZBCS is financially supported under the program of Minister of Science and Higher Education "Regional Initiative of Excellence" in years 2019-2022, Grant No 002/RID/2018/19. The TNBCC was supported by: a Specialized Program of Research Excellence (SPORE) in Breast Cancer (CA116201), a grant from the Breast Cancer Research Foundation, a generous gift from the David F. and Margaret T. Grohne Family Foundation. The UCIBCS component of this research was supported by the NIH [CA58860, CA92044] and the Lon V Smith Foundation [LVS39420]. The UKBGS is funded by Breast Cancer Now and the Institute of Cancer Research (ICR), London. ICR acknowledges NHS funding to the NIHR Biomedical Research Centre. The UKOPS study was funded by The Eve Appeal (The Oak Foundation) and supported by the National Institute for Health Research University College London Hospitals Biomedical Research Centre. The USRT Study was funded by Intramural Research Funds of the National Cancer Institute, Department of Health and Human Services, USA. CIMBA CIMBA: The CIMBA data management and data analysis were supported by Cancer Research – UK grants C12292/A20861, C12292/A11174. ACA is a Cancer Research -UK Senior Cancer Research Fellow. GCT and ABS are NHMRC Research Fellows. The PERSPECTIVE project was supported by the Government of Canada through Genome Canada and the Canadian Institutes of Health Research, the Ministry of Economy, Science and Innovation through Genome Québec, and The Quebec Breast Cancer Foundation. BCFR: UM1 CA164920 from the National Cancer Institute. The content of this manuscript does not necessarily reflect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government or the BCFR. BFBOCC: Lithuania (BFBOCC-LT): Research Council of Lithuania grant SEN-18/2015 and Nr. P-MIP-19-164. BIDMC: Breast Cancer Research Foundation. BMBSA: Cancer Association of South Africa (PI Elizabeth J. van Rensburg). CNIO: Spanish Ministry of Health PI16/00440 supported by FEDER funds, the Spanish Ministry of Economy and Competitiveness (MINECO) SAF2014-57680-R and the Spanish Research Network on Rare diseases (CIBERER). COH-CCGCRN: Research reported in this publication was supported by the National Cancer Institute of the National Institutes of Health under grant number R25CA112486, and RC4CA153828 (PI: J. Weitzel) from the National Cancer Institute and the Office of the Director, National Institutes of Health. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. CONSIT TEAM: Associazione Italiana Ricerca sul Cancro (AIRC; IG2014 no.15547) to P. Radice. Funds from Italian citizens who allocated the 5 × 1000 share of their tax payment in support of the Fondazione IRCCS Istituto Nazionale Tumori, according to Italian laws (INT-Institutional strategic projects '5 × 1000') to S. Manoukian. UNIROMA1: Italian Association for Cancer Research (AIRC; grant no. 21389) to L. Ottini. DFKZ: German Cancer Research Center. EMBRACE: Cancer Research UK Grants C1287/A10118 and C1287/A11990. D. Gareth Evans and Fiona Lalloo are supported by an NIHR grant to the Biomedical Research Centre, Manchester (IS-BRC-1215-20007). The Investigators at The Institute of Cancer Research and The Royal Marsden NHS Foundation Trust are supported by an NIHR grant to the Biomedical Research Centre at The Institute of Cancer Research and The Royal Marsden NHS Foundation Trust. Ros Eeles and Elizabeth Bancroft are supported by Cancer Research UK Grant C5047/A8385. Ros Eeles is also supported by NIHR support to the Biomedical Research Centre at The Institute of Cancer Research and The Royal Marsden NHS Foundation Trust. FCCC: NIH/NCI grant P30-CA006927. The University of Kansas Cancer Center (P30 CA168524) and the Kansas Bioscience Authority Eminent Scholar Program. A.K.G. was funded by R0 1CA140323, R01 CA214545, and by the Chancellors Distinguished Chair in Biomedical Sciences Professorship. Ana Vega is supported by the Spanish Health Research Foundation, Instituto de Salud Carlos III (ISCIII), partially supported by FEDER funds through Research Activity Intensification Program (contract grant numbers: INT15/00070, INT16/00154, INT17/00133), and through Centro de Investigación Biomédica en Red de Enferemdades Raras CIBERER (ACCI 2016: ER17P1AC7112/2018); Autonomous Government of Galicia (Consolidation and structuring program: IN607B), and by the Fundación Mutua Madrileña (call 2018). GC-HBOC: German Cancer Aid (grant no 110837, Rita K. Schmutzler) and the European Regional Development Fund and Free State of Saxony, Germany (LIFE - Leipzig Research Centre for Civilization Diseases, project numbers 713-241202, 713-241202, 14505/2470, 14575/2470). GEMO: Ligue Nationale Contre le Cancer; the Association "Le cancer du sein, parlons-en!" Award, the Canadian Institutes of Health Research for the "CIHR Team in Familial Risks of Breast Cancer" program, the French National Institute of Cancer (INCa) (grants AOR 01 082, 2013-1-BCB-01-ICH-1 and SHS-E-SP 18-015) and the Fondation ARC pour la recherche sur le cancer (grant PJA 20151203365). GEORGETOWN: the Survey, Recruitment and Biospecimen Shared Resource at Georgetown University (NIH/NCI grant P30-CA051008) and the Fisher Center for Hereditary Cancer and Clinical Genomics Research. HCSC: Spanish Ministry of Health PI15/00059, PI16/01292, and CB-161200301 CIBERONC from ISCIII (Spain), partially supported by European Regional Development FEDER funds. HEBCS: Helsinki University Hospital Research Fund, Academy of Finland (266528), the Finnish Cancer Society and the Sigrid Juselius Foundation. HEBON: the Dutch Cancer Society grants NKI1998-1854, NKI2004-3088, NKI2007-3756, the Netherlands Organization of Scientific Research grant NWO 91109024, the Pink Ribbon grants 110005 and 2014-187.WO76, the BBMRI grant NWO 184.021.007/CP46 and the Transcan grant JTC 2012 Cancer 12-054. HUNBOCS: Hungarian Research Grants KTIA-OTKA CK-80745 and NKFI_OTKA K-112228. HVH (University Hospital Vall d'Hebron) This work was supported by Spanish Instituto de Salud Carlos III (ISCIII) funding, an initiative of the Spanish Ministry of Economy and Innovation partially supported by European Regional Development FEDER Funds: FIS PI12/02585 and PI15/00355. ICO: The authors would like to particularly acknowledge the support of the Asociación Española Contra el Cáncer (AECC), the Instituto de Salud Carlos III (organismo adscrito al Ministerio de Economía y Competitividad) and "Fondo Europeo de Desarrollo Regional (FEDER), una manera de hacer Europa" (PI10/01422, PI13/00285, PIE13/00022, PI15/00854, PI16/00563, P18/01029, and CIBERONC) and the Institut Català de la Salut and Autonomous Government of Catalonia (2009SGR290, 2014SGR338, 2017SGR449, and PERIS Project MedPerCan), and CERCA program. IHCC: PBZ_KBN_122/P05/2004. ILUH: Icelandic Association "Walking for Breast Cancer Research" and by the Landspitali University Hospital Research Fund. INHERIT: Canadian Institutes of Health Research for the "CIHR Team in Familial Risks of Breast Cancer" program – grant # CRN-87521 and the Ministry of Economic Development, Innovation and Export Trade – grant # PSR-SIIRI-701. IOVHBOCS: Ministero della Salute and "5 × 1000" Istituto Oncologico Veneto grant. IPOBCS: Liga Portuguesa Contra o Cancro. kConFab: The National Breast Cancer Foundation, and previously by the National Health and Medical Research Council (NHMRC), the Queensland Cancer Fund, the Cancer Councils of New South Wales, Victoria, Tasmania and South Australia, and the Cancer Foundation of Western Australia. MAYO: NIH grants CA116167, CA192393 and CA176785, an NCI Specialized Program of Research Excellence (SPORE) in Breast Cancer (CA116201), and a grant from the Breast Cancer Research Foundation. MCGILL: Jewish General Hospital Weekend to End Breast Cancer, Quebec Ministry of Economic Development, Innovation and Export Trade. Marc Tischkowitz is supported by the funded by the European Union Seventh Framework Program (2007Y2013)/European Research Council (Grant No. 310018). MSKCC: the Breast Cancer Research Foundation, the Robert and Kate Niehaus Clinical Cancer Genetics Initiative, the Andrew Sabin Research Fund and a Cancer Center Support Grant/Core Grant (P30 CA008748). NCI: the Intramural Research Program of the US National Cancer Institute, NIH, and by support services contracts NO2-CP-11019-50, N02-CP-21013-63 and N02-CP-65504 with Westat, Inc, Rockville, MD. NNPIO: the Russian Foundation for Basic Research (grants 17-54-12007, 17-00-00171 and 18-515-45012). NRG Oncology: U10 CA180868, NRG SDMC grant U10 CA180822, NRG Administrative Office and the NRG Tissue Bank (CA 27469), the NRG Statistical and Data Center (CA 37517) and the Intramural Research Program, NCI. OSUCCG: was funded by the Ohio State University Comprehensive Cancer Center. PBCS: Italian Association of Cancer Research (AIRC) [IG 2013 N.14477] and Tuscany Institute for Tumors (ITT) grant 2014-2015-2016. SMC: the Israeli Cancer Association. SWE-BRCA: the Swedish Cancer Society. UCHICAGO: NCI Specialized Program of Research Excellence (SPORE) in Breast Cancer (CA125183), R01 CA142996, 1U01CA161032 and by the Ralph and Marion Falk Medical Research Trust, the Entertainment Industry Fund National Women's Cancer Research Alliance and the Breast Cancer research Foundation. UCSF: UCSF Cancer Risk Program and Helen Diller Family Comprehensive Cancer Center. UKFOCR: Cancer Researc h UK. UPENN: National Institutes of Health (NIH) (R01-CA102776 and R01-CA083855; Breast Cancer Research Foundation; Susan G. Komen Foundation for the cure, Basser Research Center for BRCA. UPITT/MWH: Hackers for Hope Pittsburgh. VFCTG: Victorian Cancer Agency, Cancer Australia, National Breast Cancer Foundation. WCP: Dr Karlan is funded by the American Cancer Society Early Detection Professorship (SIOP-06-258-01-COUN) and the National Center for Advancing Translational Sciences (NCATS), Grant UL1TR000124. ; Peer Reviewed
General Abstract 1. Introduction Nowadays, it is essential to develop and find new ways to reduce the increasing pollution deriving from anthropogenic and environmental sources. Human activities are major responsible of climate changes and ecosystems alterations, because of the increasing release of CO2 and other harmful gases inside the atmosphere. In order to reduce the environmental impact of the human society, a great attention is now given to such processes able to reduce the pollutants concentration in both air and water systems. Advanced oxidation processes (AOPs), which involves the generation of highly reactive hydroxyl radicals (OH•), have emerged as promising air and water treatment technology for the degradation or mineralization of a wide range of pollutants. Titanium dioxide (TiO2) induced photocatalysis is an example of AOP processes and it has been demonstrated its efficiency in the decomposition of various organic contaminants. TiO2 is a very well known and well-researched material due to the stability of its chemical structure, biocompatibility, physical, optical, and electrical properties. TiO2-based photocatalysts are used for a variety of applications such as degradation of volatile organic compounds (VOCs) [1] and decomposition of nitrogen pollutants (NOx) [2] or also organic dyes, like Methylene Blue [3]. The crystalline forms of TiO2 are anatase, rutile and brookite. In general, TiO2 is preferred in anatase form because of its high photocatalytic activity, non-toxicity, chemically stability; moreover, it is relatively inexpensive. For a long time, new synthetic routes have been developed to prepare nano-TiO2 samples in order to enhance their photocatalytic efficiency [4-6]. In fact, since many years the attention has been focused on ultrasmall semiconductive particles, because they show peculiar and enhanced properties compared to the micrometric particles ones [7]. Nano-sized TiO2 is extremely efficient towards the photodegradation processes; in particular, photo-redox reactions are greatly enhanced thanks to the high numbers of active sites present on the extremely large surface area [8]. However, in recent years many papers published the possible health risks correlated with nano-sized materials [9,10]. The small size, shape, solubility and agglomeration degree of nano-sized materials, make them able to cross the cell boundaries or pass directly from the lungs into the blood stream and finally reach all the organs in the body [11]. On the other hand, larger particles are adsorbed by organs and cells with more difficulty. The main question is then if it is necessary to use the nano-sized particles in an exclusive way. Kwon et al. [12] stated that nanocatalysts having small particle size, high surface area, and a high density of surface coordination unsaturated sites offer improved catalytic performance over microscale catalysts but this does not imply the impossibility a priori to use these latter in selected conditions. The use in photocatalysis of TiO2 powders with larger-sized crystallites is a very interesting approach to reduce the possible health problems caused by nanoparticles. 2. Aims of work The aims of this PhD work is to evaluate the photoactivity of micro-TiO2 samples using as irradiation source both UV and LED lights. At first, commercial powdered micro- and nano-sized TiO2 catalysts, were tested and then improved for the degradation of pollutants in both gas and aqueous phase. The ultimate purpose of the PhD work is to test the possibility of using TiO2 for production of building materials; the photocatalytic activity of TiO2 can be then exploited for degrading air pollutants inside domestic environments or workplaces, thus making them healthier over time. Application of photocatalysis to construction buildings began towards the end of 1980s with the production of photocatalytic glasses, which provided self-cleaning and anti-fogging properties [13]. Afterward photocatalytic cementitious materials have been patented by Mitsubishi Corp. and Italcementi SpA [14,15]. In all these construction materials, the active photocatalyst is anatase TiO2. Although the use of photocatalytic cement is still restricted and limited, many buildings and city roads have been designed and constructed since 2000. Relevant examples are Church "Dives in Misericordia", Rome, Italy; Music and Arts City Hall, Chamberéry, France [16]. In general, the mostly used powders of commercial TiO2 for photocatalytic applications are nanometric: this leads some advantages in terms of pollutants degradation efficiency, but many backwards too, like the difficulty to recover the catalyst or the possibility of inhalation with consequent health damage, even the high cost is not negligible. For this reasons, the optimization of the photocatalytic efficiency of micrometric compounds is desired, in order to replace definitely the nanometric catalysts. In this PhD work micro-sized TiO2 powder was used for the preparation of porcelain gres tiles, which are commercial manufactured products, opening a new generation of material intrinsically safer than the traditional photocatalytic products. All samples were fully characterized investigating textural, structural, morphological and surface properties. The photoefficiency was evaluated in different ways, which can be summarized as follows: • Assessment of the photoactivity of commercial samples, both nanometric and micrometric, in gas and aqueous phases in the presence of typical indoor and outdoor pollutants (NOx and Volatile Organic Compounds (VOCs), textile dyes, surfactants); • Assessment of the self-cleaning effect, evaluated by water contact angle measurements, during ultraviolet irradiation on micro-TiO2 tiles of building materials on whose surface the oleic acid is deposited (ISO/WD 27448-1); • Assessment of the effects of the addition of anionic or cationic ions, like fluorine, tin, rhenium or tungsten, on the catalytic surface through the impregnation method. Doping is useful to lower the titanium band gap and accordingly to increase the photocatalytic activity of the material. 3. Experimental details 3.1 Catalytic materials a) Preparation of TiO2 powders Different commercially available micro- and nano-sized pigmentary-powdered TiO2 were chosen; the catalysts were characterized and used without further treatment. In the Table 3.1 the photocatalytic powders used in this PhD work are reported. For each powder, the different physico-chemical characteristics are specified: XRD for the crystalline nature, BET for the surface area, XPS for the atomic composition of elements, SEM and TEM for the particles morphology, FTIR for the chemical composition of samples supported with DRS (diffuse reflectance spectra) for the characterization of the light absorption features and band-gap determinations. Before starting the photooxidation process of pollutants, commercial TiO2 powders were deposited in two plains of glass sample (each plain of 7.5x2.5 cm2). TiO2 powders (0.050 g) were first suspended in 2-propanol (50 ml) so to obtain a homogeneous suspension and then deposited by drop casting onto one side of the laminas. The solvent was simply evaporated at room temperature without any further treatment. The samples consisted in a thicker layer, obtained by overlapping three TiO2 coatings (labelled as T, standing for triple layers, followed by the substrate abbreviation), as shown in previous works by Bianchi et al. [17,18]. Table 3.1. Main features of TiO2-based commercial powders, used as photocatalysts, with the corresponding crystalline phase: nanometric and micrometric samples. Powder Crystalline phase BET (m2/g) Micro/Nano XPS OH/Otot P25 (Evonik) 75% anatase; 25% rutile 52 NANO 0.14 PC105 (Crystal) anatase 80 NANO 0.85 1077 (Kronos) anatase 11 MICRO 0.32 AH-R (Hundsman) anatase 12 MICRO 0.19 AT-1 (Crystal) anatase 12 MICRO 0.24 1001 (Kronos) anatase 11 MIXED PHASE (micro+nano) 0.27 1002 (Kronos) anatase 9 MIXED PHASE (micro+nano) 0.35 1071 (Kronos) anatase 10 MIXED PHASE (micro+nano) 0.18 A-Z (Hombitam) 99% anatase 4 MICRO 0.25 AN (Hombitam) 98,5% anatase 12 MICRO 0.5 N.10 (HombiKat) 98% anatase; 2% rutile 13 MICRO 0.13 b) Preparation of vitrified tiles Among all building materials, commercially available white tiles by GranitiFiandre SpA (sample name White Ground Active® (WGA) or Orosei Active) were chosen and used for the preparation of photocatalytic tiles. Porcelain gres tiles are manufactured under high pressure by dry-pressing of fine processed ceramic raw materials, with large proportions of quartz, feldspar, and other fluxes. The body of these materials is then fired at very high temperatures (1200–1300◦C) in kilns [19]. After impregnation with water, the tiles are subjected to temperature cycles between +5 and -5 °C, during a minimum of 100 freeze–thaw cycles, in order to verify their resistance to the frost and their durability. No evident cracks or damages were observed on the samples. The final material is thus characterized by lack of porosity, complete water-proofing, durability, hardness, wear resistance properties, and a complete frost resistance. The porcelain gres tiles were covered at the surface with a mixture of micro-TiO2 and a commercial SiO2-based compound prepared via ball–mill [20,21]. To achieve the desired product stability, at the end of the preparation procedure tiles were treated at high temperature (680 °C) for 80 min and then brushed to remove the powder present at the surface and not completely stuck. Temperature was precisely chosen to maintain the anatase form of the semiconductor and allow the vitrification of the tiles surface. Tiles were also prepared with the same procedure but without adding the photoactive oxide into the SiO2-based compound for the sake of comparison (sample name White Ground (WG) or Orosei)). The surface wettability of photoactive porcelain gres tiles was evaluated by static contact angle (CA) measurements performed with an OCA20 instrument (DataPhysics Co., Germany) equipped with a CCD camera and a 500 μL-Hamilton syringe to dispense liquid droplets. [22,23]. c) Doping effect on TiO2 powders Micrometric TiO2 powders were doped with cations like tungsten (W), tin (Sn) and rhenium (Re), and fluoride anions (F-). This was done with the aim to improve the photoefficiency of the micro-sized TiO2 catalysts, which have lower activity than the traditional nanopowders. Ren at al. [24] demonstrated that the fluorination of TiO2 nanocrystals gave a photocatalytic enhancement due to the higher separation efficiency of photogenerated electrons and holes. Furthermore, it has been found that the surface fluorination favors the generation of free OH radicals, which are responsible of an enhanced oxidation [25]. Regarding the doping with metal cations, in the literature is reported that Re dopant could effectively inhibit the recombination of the photoinduced electrons and holes [26]. Re can act as electron trap and promote the interfacial charge transfer processes in the composite systems, which reduces the recombination of photoinduced electron-hole pairs, thus improving the photocatalytic activity of TiO2. Moreover, it was demonstrated that that metal particles doping can facilitate the electron excitation by creating a local electrical field, enhancing photoinduced surface redox reactions: it results in the extension of the wavelength of TiO2 response towards the visible region [27]. The band gap energy of the doped-TiO2 results less than that of naked TiO2, which induces the red shift of the adsorption edge to respond to visible light. This peculiar feature gets interesting for the use of LED (Light Emission Diode) as irradiation source for the photooxidation processes, because LED emissions are located only in the visible region of light. In fact, an important aspect is the use of irradiation by visible light, through LED lamps. Several cities, like Milano, Stockholm, Los Angeles, Copenhagen, have chosen to adopt the LED emission for the outdoor illumination: Milano will substitute the 80% of urban illumination with the LED light within May 2015 (Expo start date). Advantages, connected to this emerging technology (high durability, cheapness, low energy consume), adhere very well with the environmental safety. Thus, NOx and VOCs photodegradation was performed with LED lamp, using micrometric doped powder. The classical impregnation method was applied to dope the catalyst surface with fluoride anions, starting from inorganic fluoride salts (NaF, NH4F, CaF2 and F2). At the end of the impregnation procedure (24 h, room temperature), powders were calcined at 400°C for 4 h and rinsed in distilled water three times. The metal doping was performed in two different ways: it was used the same procedure of impregnation method for tin (Sn) surface doping, whereas a different surface deposition technique (decoration method) was performed for metals of tungsten (W) and rhenium (Re). Decoration of M- or MO-NPs is commonly implemented by means of ultra-sounds (US) in aqueous or organic solutions where ceramics or polymer substrate powders are dispersed [28]. In the latter case, the precursor of metal was sonicated at a costant temperature of 80°C for 3 h, with 33.0% amplitude and a 50 W cm-2 intensity. At the end, the solution was centrifugated many times to remove all the solvent; the final powders was washed with n-pentane and centrifugated again. The residual solvent was evaporated and the sample was finally calcined at 480°C for 40 h to completely remove the organic scents. 3.2 Testing procedure a) Photocatalytic set-up in gas-phase Photocatalyitc degradation of air pollutants, such as acetone, acetaldehyde, toluene (well known as VOCs) and NOx, were conducted in Pyrex glass cylindrical reactors having different volume depending on the type of analyzed pollutant: 5 L for VOCs and 20 L for NOx, respectively. In the case of VOCs analysis, the gaseous mixture in the reactor was obtained by mixing hot chromatographic air (f.i. 250 ◦C for toluene), with relative humidity (RH) of 40%, and a fixed amount of volatilized pollutant, in order to avoid condensation. The initial concentration of VOCs in the reactor was 400 ppmv, monitored directly by micro-GC sampling. Photon sources were provided by a 500 W iron halogenide lamp (Jelosil, model HG 500) emitting in the 315–400 nm wavelength range (UV-A) at 30 Wm−2 or by a LED lamp, emitting into the visible region. Acetone and acetaldehyde degradation tests lasted for 2 h, whereas toluene tests for 6 h, due to the difficulty in degrading a molecule with an aromatic ring and with a complex degradation pathway [19]. For NOx photodegradation study, a first static experimental setup was obtained used the following conditions: RH: 50%, UV light of 10 Wm-2 (for TiO2 powders deposited on glass sheets) or 20 Wm-2 (for micro-sized TiO2 gres tiles), with a NOx starting value of 1000 ppb. The analytical procedure was reported by Bianchi et al. [21]. NOx degradation by TiO2 powders (always immobilized on a glass sheet) and photoactive tiles was conducted also in continuous conditions using a plug-flow reactor (with an effective volume of 0.025 L) built strictly following the ISO 22197-1 rule [29]. Experimental conditions were maintained as follows: RH: 40%, 20Wm−2, [NOx]inlet=500 ppb, and 180, 32.4, 9, and 4.2 L h−1 total flow, respectively. A chemiluminescent analyzer (Teledyne Instruments M200E) was used to check the conversion of the pollutant in both batch and plug-flow reactor setups. b) Photocatalytic set-up in aqueous-phase The photocatalytic apparatus was a 1 L glass stirred reactor equipped with an iron halogenide UV lamp (500 W, Jelosil® HG500) emitting light at wavelengths of 315–400 nm and able to irradiate the reactor with a specific power of 95 Wm-2, when TiO2 powder was used as catalyst. The UV lamp was placed beside the reactor, which was cooled with water at a temperature of 30 ± 0.5◦C, as reported previously by Gatto et al. [30]. TiO2 was introduced in the reactor at the beginning of each test (0.66 g/L for surfactant degradation and 0.1 g/L for textile dyes). The variation of the surfactant (PFOA) concentration in solution was monitored by total organic carbon (TOC) analysis and ionic chromatography. The PFOA initial concentration ([PFOA]0= 4 mM) was maintained lower than its critical micellar concentration (7.8 mM) in order to avoid the formation of emulsions during the kinetic tests. Samples (10 mL) of the reaction mixture were collected at different reaction times: typically at 0 min (before the start of the reaction), 30 min, 1 h, 2 h, 3 h, 4 h, 6 h and 9 h. Textile dyes, chosen for the photodegradation tests, were Rhodamine B (RhB), Methylene Blue (MB) and Crystal Violet (CV); dyes degradation was checked every 60 min by determining the dye concentration in the water solution by a UV–vis spectrophotometer analyzer (T60 UV–vis PG LTD instruments), using water as the reference. Pure CV has an absorbance maximum at 590 nm, RhB at 555 nm and MB around 670 nm. Textile dyes degradation was also performed using photoactive tiles, covered with the micrometric 1077 powder. For this aim, a cylindrical batch reactor of 1 L volume was used for dye degradation tests in presence of ten photoactive tiles (0.03 m2 total surface photoactive area) immersed into the liquid solution, as reported by Bianchi et al. [31]. Refrigeration was allowed by a cooling jacket. Two different lamps directly immersed into the dye solution were used with this setup: a typical germicidal 9 W UV-C lamp (Philips TUV BL-S, model AEPL-7913 mercury vapor low pressure), with a radiant power of 1 Wm-2 and a 125 W UV-A lamp (Jelosil, mercury vapor low pressure), with an illuminance of 65 Wm-2, in correspondence of the tiles surface. During photocatalytic tests, the TiO2 active faces of the tiles were turned towards the UV light. After each test, the tiles were simply washed using deionized water and acetone and then left in deionized water all night long. The same dyes solution (RhB, MB, CV) were used in the present setup at a concentration of 1 × 10−5 M. c) Self-cleaning effect The self-cleaning capability of TiO2 photoactive tiles was evaluated in two different ways: (1) through the measurement of the water contact angle (CA) (KRUSS GmbH) of a tile, after oleic acid deposition and UV irradiation (Jelosil, model HG 500) for 76 h and (2) through the monitoring, by a colorimeter, of the discoloration of dyes directly put on the tiles surfaces, after exposure to the sunlight (Milan – Italy, May 2012). For water CA measurements, a test piece of porcelain gres tile of 100 ± 2mm2 were pre-treated by ultraviolet irradiation of 20 Wm-2 for at least 24 hours. Then, the catalytic samples were dipped inside an oleic acid (Fluka, >80%) solution (0.5 vol%) in order to simulate a polluting condition. The presence of oleic acids on the tile surface modify its wettability. After UV irradiation it was measured the CA at an appropriate time interval, observing a continuous decrease of the CA values related to a degradation of the polluting agent. The measurement can be considered concluded when the contact angle value of the clean photocatalytic tile is restored, as before the oleic acid deposition. For comparison, the measurement is repeated on a sample similarly polluted with oleic acid, but left in the dark for 76 hours. Furthermore, it was taken a sample of porcelain gres tile, not containing TiO2, and it was immersed into oleic acid solution and irradiated, with the aim to evaluate the pure contribute of UV irradiation. Dyes degradation instead was monitored by Vis-spectrometer equipped with an integrated sphere (OceanOptics, USB400-VIS-NIR-ES). 1 μL of dyes, dissolved in water, was put on the tiles surface and left under the sunlight, whose power was continuously checked from 9 am to 5 pm every day by a radiometer DeltaOhm HD2012,2. A mean power irradiation value of 7.28 W/m2 was measured. The color analysis was performed using the CIEXYZ and CIELAB models [22]. 4. Results and discussion 4.1 Characterization results a) Powders characterization Anatase, evidenced by XRD patterns, is the unique polymorph present for all samples, except for P25 and N.10 (by Hombikat) powders, which exhibit even the rutile phase (25 and 2%, respectively). The crystallographic reflexes (1 0 1), (2 0 0) and (2 1 1) have been employed to calculate the average crystallites size of the various titania particles. P25 and PC105, commercial nanometric powders, have comparable crystallite size centered on 25 nm, while the other samples have values between 120 and 200 nm, confirming their micro-sized nature. These structural properties are reflected in their BET surface areas that are about 11-12 m2/g, which are much lower compared to the nano-sized ones (Table 3.1). For 1001, 1002, 1071 samples Sherrer calculation was not performed, as TEM analysis reveals the presence of both micro-sized and ultrafine fractions, as it is visible in Fig. 4.1, section d. HR-TEM and SEM images confirmed the average crystallites sizes extrapolated by XRD analysis; moreover, it was excluded the presence of ultrafine particles in 1007, AT-1, AH-R, A-Z, AN and N.10 powders. It can be evidenced that nano-sized materials perfectly fall within the "nano" definition: in fact, both samples are characterized by average particles size of 15-30 nm (Fig. 4.1, section a), closely packed features and roundish contours [19]. As for what concerns the other powders (1077, AT-1, AH-R, A-Z, AN, N.10), they all exhibit well crystallized particles possessing smooth edge and average diameter size in the 120-200 nm range (see Fig. 4.1, section b and c), with fringes patterns belonging to the TiO2 anatase polymorph. On the contrary, for 1001, 1002 and 1071 powders TEM images again confirm that they are composed by a mixture of both micro-sized crystallites and some ultrafine particles (Fig. 4.1, section d). The surface state of the TiO2 particles was analyzed by XPS. No significant differences can be appreciated in the Ti 2p region among all the present samples concerning the binding energies (BE) and the full width at half-maximum (FWHM) values. The peak of Ti 2p3/2 is always regular and the BE at about 458.5 ± 0.1 eV compares well with the data for Ti(IV) in TiO2 materials [32]. The analysis of the oxygen peaks exhibits the presence of more than one component, which can be attributed to lattice oxygen in TiO2 (529.9 eV) and to surface OH species (>531.5 eV) respectively. A particular O1s shape was observed for PC105. In this case, the OH component is very intense probably due to a particular industrial synthesis in order to enhance the photocatalytic efficiency of the sample. The hydrophilicity/hydrophobicity character of photocatalysts surface plays a crucial role in determining the adsorption step and thus the photocatalytic activity, at least in the degradation of pollutants [33]. P105 exhibits the highest concentration of OH that represent the 85% of the oxygen at the surface, as it shown in Fig. 4.2. It is noteworthy that the micro-sized samples, with the exception of N.10 (by HombiKat) sample, present a higher atomic concentration of OH groups in comparison with P25, pointing out the higher hydrophilic character of their surface (see Table 3.1, fifth column). Fig. 4.1. TEM images of the various TiO2 powders. Section a: P25; section b: 1077; section c: AH-R; section d: 1071. FTIR spectra in the ν(OH) spectral range of the samples in air revealed two complex absorption bands, respectively located in the 3000–3450 cm-1 range and at ν ≥ 3600 cm-1. Based on the spectral behavior and of our previous data [19], the former envelope can be ascribed to the stretching mode of all H-bonded OH groups present at the surface of the various solids, whereas the latter corresponds to the stretching mode of all Ti–OH species free from hydrogen bonding interactions [34]. It is well-known that surface hydroxyl radicals play a fundamental role in the photocatalytic processes [35]. In particular, photo-generated holes react with water molecules adsorbed on TiO2 surface, leading to the formation of OH•: TiO2 + hν → h+ + e- (3.1) h+ + H2O → OH• + H+ (3.2) The pigmentary TiO2 powders showed appreciable amounts of OH groups and this validate their rather good performances in the photocatalyitc degradation, as reported in our previous study [19]. Fig. 4.2. O1s XPS spectra for (a) P25; (b) PC105; (c) 1077; (d) AT-1. b) Gres tiles characterization XPS measurement reveals the presence of only Ti(IV) and a Ti/Si ratio of 0.15 for the micro-TiO2+SiO2-based compound, which belongs to porcelain grès tiles. The preservation of the pure anatase form was verified by both XRPD and XPS measurements. As reported by Anderson and Bard [37] the presence of SiO2, together with TiO2, enhances the formation of hydroxyl radical OH•, which may be achieved via strong Brønsted acid sites at the TiO2/SiO2 interface region. Such incorporation inhibits the crystal growth of TiO2 allowing the preservation of the anatase structure at high temperature. By the investigation of morphological features, the presence of SiO2-based compound is evident in gres tiles (Fig. 4.3), in the form of either small protruding particles or as amorphous coating which covers the TiO2 particles. Fig. 4.3. HR-TEM images of the TiO2 porcelain gres tiles materials. (a) refers to low magnification and (b) to high magnification. The very thin nature of these particles and/or coating allows to inspect the fringe patterns located below, confirming that the spacing among the fringes are still ascribable to the anatase TiO2 polymorph. 4.2 Photocatalytic tests 4.2.1 Photocatalytic activity in gas-phase a) NOx photoabatement with TiO2 powders In this section, several commercial pigmentary powders were tested for NOx degradation and were compared with the nanometric powders efficiency (P25 and PC105). At first, the tested concentration of NOx in the reactor was 1000 ppb, in order to follow the same pollutant concentration requested by the ISO 22197-1 rules [38]. All the samples showed good photocatalytic performances, because the abatement of NOx was early completed at the end of 3 hours, except the 1071 (by Kronos) sample, which showed lower photodegradation (61.5 %). The efficiency of the other samples was between 90 and 99%: this behavior leads to hypothesize a complete degradation of the pollutant within the chosen limited time of the run (3 h). In particular, it is interesting to observe the photodegradation trend of the only micro-sized samples (1077, AH-R, Hombitam A-Z, Hombitam AN and HombiKat N.10) at 15 min, 30 min, 60 min and 240 min, the most significantly times. In Fig. 4.4 we can observe the peculiar differences, which arise in the initial period of the degradation. 1077, Hombitam AZ and Hombitam AN seem to be the most active, showing the best efficiency in the first times of reaction (15, 30 min). This behavior can be explained through the physico-chemical features and the amount of hydroxyl radicals that initiate the oxidation of NO. The ratio of OH/Otot, obtained by XPS analysis, resulted to be, in fact, higher than the other micrometric ones (Table 3.1). In particular, after 2 h, the NOx conversion of these samples is higher than 90%, very close to that of P25, which reaches the complete pollutant degradation in the same time. Thus, even if the nano-sized materials (P25 and PC105) show the best performances, the photocatalytic activities of the pigmentary powders are comparable, in agreement with the presence of appreciable amount of surface hydroxyls, which are crucial species for the photooxidation processes [39]. From the trend in the Fig. 4.4 it is clear that the micrometric samples with the best photocatalytic performances are the ones showing the largest OH component, the following 1007, Hombitam AZ and Hombitam AN. Fig. 4.4. TiO2 commercial micro-sized powders (1077, AH-R, Hombitam AZ, Hombitam AN, HombiKat N.10) for NOx abatement at 15, 30, 60, 240 min under UV light irradiation. b) NOx photoabatement with photoactive tiles Another study concerns the application in photocatalysis of building materials. In this PhD work porcelain gres tiles, covered with micrometric TiO2 powder, were used for the NOx degradation, under UV light, in static experimental conditions in gas phase. Starting from 1000 ppb of NO2, i.e. the same amount required by the ISO 22197-1 specification, the 65% of degradation was measured after 6 h. A very interesting trend (Fig. 4.5) was observed also following the NO2 degradation by photocatalytic tiles. NO2 was chosen as specific reference pollutant instead of the more generic NOx, because of its higher hazardousness. The continued exposure to high NO2 levels, in fact, can contribute to the development of acute or chronic bronchitis [40]. More in detail, tests were carried out by using as starting pollutant concentration 106 ppb (value not to be exceeded more than 18 times in a calendar year), and 212 ppb (alert threshold), according to the Directive 2008/50/EC of the European Parliament, which states the guidelines for the protection of the human health. It is possible to observe (Fig. 4.5) that, as the amount of starting pollutant is decreased, the time necessary to bring its concentration under the limit required by the European Directive (21 ppb) also decreases. In the Fig. 4.5 inset the degradation trend can be observed in the case of an initial pollutant concentration close to the alert threshold. Fig. 4.5. Time necessary to degrade the pollutant and decrease its amount under the limit value required by the Directive 2008/50/EC of the European Parliament and of the council on ambient air quality and cleaner air for Europe (21 ppb); 20 W/m2, RH 50%, static conditions. Therefore under real pollution conditions, simulating a day in the absence of wind (static conditions) WGA is able to degrade NO2 in a very efficient way bringing the pollutant concentration down to the required limit (21 ppb) in a matter of hours [21]. Micro-sized TiO2 porcelain gres tiles were also tested in continuous conditions using a plug-flow reactor, whose the operating conditions have been softened cutting the inlet concentration by half (500 ppb, instead of 1000 ppb). It was investigated the role of the flow per hour on the final NO2 conversion. An interesting aspect revealed: the modification of the flow per hour leads to an evident change of the contact times that is the time the pollutant can stay "in contact" with the catalyst surface. As expected, increasing the contact time, the final conversion proportionally increases. This result is very evident for Orosei Active sample that shows a conversion varying from 1.3% to 82.0% at 180 L h−1 and 4.2 L h−1, respectively. The obtained 82% conversion at 4.2 L h−1 flow can be consequently considered a very good value. c) VOCs photoabatement with TiO2 powders In order to study the photocatalytic activity of nano- and micro-sized samples, the degradation of three different VOCs, acetone, acetaldehyde and toluene, has been performed. As an illustrative example, it was reported the toluene photodegradation tests. For both nano-and micro-sized TiO2 powders, the pollutant was not completely degraded, even after 6 h of reaction. Moreover, it is noteworthy that the degradation percentages fell more or less in the same range (46–52%) with a slightly higher value for the nanometric P25 and PC105 catalysts, as it is shown in Fig. 4.6. Toluene degradation resulted very difficult due to the complexity of molecule, which presents the aromatic ring. The different catalysts show similar behavior toward the toluene degradation, irrespective of their physico-chemical characteristics. On the contrary, the pollutant mineralization is rather different for almost all samples. Furthermore, a low amount of CO2 formation confirmed the incompleteness of the degradation reaction. The possible by-products, which could take form during the degradation, were monitored by FTIR measurements. After the employment in toluene degradation, the spectra of the materials underwent deep changes. In particular, it was possible to recognize signals of unreacted toluene (T) and of several by-products deriving from its degradation, among which benzyl alcohol (BZOH), benzoic acid (BZAc) and benzaldehyde (BZH) [19]. In addition, the signals due to the stretching mode (νOH) of Ti-OH species free from hydrogen bonding interactions were disappeared with the parallel increase of the broad envelope generated by H-bonded OH groups [31]. Thus, it was possible to state that the catalysts surface underwent irreversible changes after the employment in the photodegradation reaction of toluene: the photo-active "free" Ti-OH sites were completely absent, as a result of their participation to the reaction. Fig. 4.6. Toluene degradation histogram: photoefficiency achieved with commercial micro-sized TiO2 and compared to the P25 and PC105 ones (nanometric). Their disappearance was a clear evidence of why toluene degradation appeared incomplete even after 6 h of reaction for all the samples, regardless of the morphological features of the materials. Therefore, in the case of toluene and in general for all less hydrophilic VOCs, it was well evident that both micro-sized materials and nano-sized ones possess almost the same photocatalytic behavior. 4.2.2 Photocatalytic activity in aqueous-phase Parallel with photocatalytic tests in gas-phase, photodegradation of surfactants and textile dyes in aqueous phase were performed. In particular, the PFOA (perfluooroctanoic acid) was chosen as surfactant species. The abatement was conducted by using P25 nano-powder as catalyst. The photodegradation trend, monitored at different times, highlighted the incomplete PFOA mineralization. For the entire duration of the photo-abatement process, it was possible to observe a decrease in the PFOA content in solution. However, the mineralization after 4 h settled down: the fluoride content and the percentage mineralization after 6 and 9 h remained equal to 29% and 32%, respectively, as reported by Gatto et al. [29]. Through HPLC-MS analysis was confirmed the presence of the intermediates in the solution that took form through two possible degradation pathways: this surface modification might influence the catalyst reducing the photocatalytic efficiency of TiO2. Nevertheless, it is important to note that, as reported in the literature, no PFOA abatement was observed working in the presence of TiO2 as photocatalyst without UV irradiation as well as under UV irradiation in the absence of photocatalyst (photolysis) [31]. The other interesting study concerns the textile dyes photodegradation, using micro-sized TiO2 (1077) powders as catalysts. The textile dyes analyzed were Methylene Blue (MhB), Rhodamine B (RhB) and Crystal Violet (CV). Experimental dark tests showed a very low adsorption of all the dyes on both kinds of powders. The contribute of photolysis was almost negligible for MhB and CV, whereas 12% of dye degradation for simple photolysis (10% for P25) was achieved for RhB. Nano-sized powder showed the best results for all the considered dyes achieving the complete decolorizing of the water solution, but also micro-sized sample was able to degrade the pollutants with a good efficiency (ranging from 48 to 58% depending on the dye in six hours) (see Fig. 4.7), as reported by Bianchi et al. [30]. In addition, the micro-sized powder can be easily filtered and recovered in order to be immediately reused for further photodegradation reactions. In fact, 1077 was recovered by the simple centrifugation and reused in the same dye degradation test with no loss of photoactivity [30]. Fig. 4.7. Photocatalysis of dyes performed with powdered micro-TiO2 catalyst (1077): crystal violet □; methylene blue ▲; rhodamine B ◌. Another application is relative to the photocatalytic efficiency of TiO2 porcelain gres tiles, evaluated through UV-vis measurements. This choice reflects the fact that photoactive porcelain gres tiles are covered with the micrometric 1077 powder. It was observed an increase of about 15% of dyes degradation in comparison to the simply photolysis. These porcelain gres tiles can be reused, just after insertion of the tiles in distilled water, and without affecting the photocatalytic activity. In fact, all the tests were done using the same batch of ten samples of industrial tiles, and no loss in their photoactivity was monitored. This indicates that the TiO2 deposited layers are not deactivated during the reaction either by loss or poisoning of the catalyst, and can be reutilized in subsequent runs. Thus, these new industrial ceramic materials are surely an interesting alternative to TiO2 suspensions in photocatalytic applications avoiding the removal of the particles at the end of the process. 4.2.3 Self-cleaning effect A different aspect for the evaluation of gres tiles photo-efficiency is the CA evaluation, measured on micro-sized TiO2 porcelain gres tiles, after the deposition of oleic acid and irradiation by UV lamp. At first, before the oleic acid (Fluka, >80%) deposition, the pretreatment CA measurements were performed obtaining value of about 31°. The, the catalytic samples were dipped inside the oleic acid solution (0.5 vol%); the presence of oleic acids on the tile surface modify its wettability, the water contact angle in fact increases to about 65°. After UV irradiation it was measured the CA at an appropriate time interval, observing a continuous decrease of the CA values related to a degradation of the polluting agent. We observed that after 76 h of irradiation, the water CA reached the starting value before the oleic acid deposition (about 30°). This highlights the self-cleaning properties of TiO2 porcelain gres tile [22] and its photocatalytic efficiency for the degradation of organic contaminant deposited on the surface. On the contrary, the same kind of porcelain gres tile (Orosei Active), treated with oleic acid, but maintained in the dark, does not show modifications of CA in the range t0 and t76. The same procedure, consisting in the deposition of oleic acid solution and irradiation under UV light for 76 h, was performed for a porcelain gres tiles, not containing TiO2. Even in this case the CA measurement during the UV irradiation remained the same, i.e., the initial CA measured on the oleic acid film (65°). It is justified that the change in the value of the contact angle is due merely to the photodegradation of the oleic acid due to both the action of UV radiation and the photocatalytic efficiency of the used material and not by spontaneous degradation of oleic acid, induced by non photocatalytic factors. Thus, the photocatalytic process is necessary for the abatement of organic pollutants [17]. 4.3 Doping effect on TiO2 powders Micro-sized 1077 powder was even doped by the impregnation method. First of all the fluorination effect was investigated, making a comparison with the corresponding nanometric P25 powder: in both powders, after the fluorination, the photocatalytic activity of NOx and VOCs abatement resulted increased. The simply surface fluorination seems to be a good method to increase the photoactivity in commercial TiO2 samples, even with large crystallites [41]. In particular, the morphological features evidenced in the HR-TEM images and FT-IR spectral patterns, showed significant features. When the fluorination was carried out on the 1077 sample, there was an increasing of the OH groups interacting by H-bonding in F2 fluorination and new families of free OH groups involving Ca2+ and Na+ ions. The simple surface fluorination by fluorination resulted as an easy and good method to increase the photoactivity in commercial TiO2 samples, even with large crystallites, as reported in Fig. 4.8. Fig. 4.8. Toluene degradation for both micro- (1077) and nano-sized (P25) TiO2 samples, naked and fluorinated (NaF precursor). Physico-chemical characterization demonstrated that the surface fluorination influenced all the surface OH groups, leaving free only some particular OH "families", reasonably the more active in the photocatalytic process. Thus, the driving force of the process is both the presence of active OH population and the efficient adsorption of the pollutant molecules on the photocatalytic semiconductor surface. Parallel with this, the metal surface deposition with Sn, W and Re lead to an improved photoefficiency. In this case, micro-sized TiO2 powders exhibited a higher photoactivity compared with the naked TiO2 one. In particular, an interesting aspect was even the evaluation of photo-efficiency of doped 1077 using the LED light as irradiation source for the pollutant degradation. It has been observed that the photo-abatement efficiency of micro-sized catalysts for VOCs is improved by the presence of metals particles, in particular in the case of rhenium and tungsten. The degradation percentage of acetone was in fact, 37% for 1077_W and 33% for 1077_Re, compared with the 1077, which showed a negligible photoactivity (~2%), when the catalysts were irradiated by visible light. In Fig. 4.9 it is possible to see the improved photo-efficiency. In fact, the metal species like W and Re have the main properties of promote the charge transfer and the visible light absorption, which lead to enhanced photocatalytic degradation of pollutants than naked micro-sized TiO2, even under visible light irradiation [42]. Fig. 4.9. Acetone photodegradation in gas-phase under visible light (performed with a LED lamp). 5. Conclusions The photocatalytic activity of both nanometric and micrometric TiO2 powders was evaluated, revealing that nano-sized powders have the best photo-efficiency. However, commercial pigmentary micro-sized TiO2 powders have given good results proving that they could be good materials in photocatalysis and good alternative to nano-sized catalysts. In particular, 1077, Hombitam AZ and AN are the micro-sized TiO2 powders with the highest photoactivity for NOx abatement. The low surface area is not a discriminant factor if other features compensate it; the ratio of OH/O has a specific influence for the pollutants photodegradation together with the morphological features of particles. In fact, nanometric P25 is characterized by a significant higher amount of hydroxyl radicals, in agreement with the optimal efficiency in pollutants photodegradation. However, also pigmentary 1077, Hombitam AZ and AN samples show appreciable amount of OH• groups and this justifies their good catalytic performance. Furthermore, porcelain gres tiles, prepared entrapping micro-TiO2 at the SiO2 surface confirmed a stable and reproducible photocatalytic activity toward organic contaminants, such as dyes and NOx, in both liquid and gas phase. This indicates that these new industrial ceramic materials with micrometric TiO2 are surely an interesting application, which avoids the use of traditional nanomaterials in powder form for their preparation. In addition, the doping of micrometric TiO2 powders with anionic or cationic species highlighted the possibility to increase the catalytic performance obtaining comparable results with naked nanometric samples. And, as a consequence of the high demand of the use of LED lamps in the indoor and outdoor areas, the metal particles on the micrometric TiO2 surface confirmed their ability to adsorb visible light and to be considered sensitizers. To summarize, powders with large particles and low surface area can have good photoefficiency for the depollution abatement.
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Quantifying the genetic correlation between cancers can provide important insights into the mechanisms driving cancer etiology. Using genome-wide association study summary statistics across six cancer types based on a total of 296,215 cases and 301,319 controls of European ancestry, here we estimate the pair-wise genetic correlations between breast, colorectal, head/neck, lung, ovary and prostate cancer, and between cancers and 38 other diseases. We observed statistically significant genetic correlations between lung and head/neck cancer (rg = 0.57, p = 4.6 × 10-8), breast and ovarian cancer (rg = 0.24, p = 7 × 10-5), breast and lung cancer (rg = 0.18, p =1.5 × 10-6) and breast and colorectal cancer (rg = 0.15, p = 1.1 × 10-4). We also found that multiple cancers are genetically correlated with non-cancer traits including smoking, psychiatric diseases and metabolic characteristics. Functional enrichment analysis revealed a significant excess contribution of conserved and regulatory regions to cancer heritability. Our comprehensive analysis of cross-cancer heritability suggests that solid tumors arising across tissues share in part a common germline genetic basis. ; he authors in this manuscript were working on behalf of BCAC, CCFR, CIMBA, CORECT, GECCO, OCAC, PRACTICAL, CRUK, BPC3, CAPS, PEGASUS, TRICL- ILCCO, ABCTB, APCB, BCFR, CONSIT TEAM, EMBRACE, GC-HBOC, GEMO, HEBON, kConFab/AOCS Mod SQuaD, and SWE-BRCA. The breast cancer genome-wide association analyses: BCAC is funded by Cancer Research UK [C1287/A16563, C1287/ A10118], the European Union ' s Horizon 2020 Research and Innovation Programme (grant numbers 634935 and 633784 for BRIDGES and B-CAST, respectively), and by the European Community's Seventh Framework Programme under grant agreement number 223175 (grant number HEALTH-F2-2009-223175) (COGS). The EU Horizon 2020 Research and Innovation Programme funding source had no role in study design, data collection, data analysis, data interpretation, or writing of the report. Genotyping of the OncoArray was funded by the NIH Grant U19 CA148065, and Cancer UK Grant C1287/ A16563 and the PERSPECTIVE project supported by the Government of Canada through Genome Canada and the Canadian Institutes of Health Research (grant GPH-129344) and, the Ministère de lÉconomie, Science et Innovation du Québec through Genome Québec and the PSR-SIIRI-701 grant, and the Quebec Breast Cancer Foundation. Funding for the iCOGS infrastructure came from: the European Community 's Seventh Framework.Programme under grant agreement n° 223175 (HEALTH-F2-2009-223175) (COGS), Cancer Research UK (C1287/A10118, C1287/A10710, C12292/A11174, C1281/A12014, C5047/A8384, C5047/A15007, C5047/A10692, C8197/A16565), the National Institutes of Health (CA128978), and Post-Cancer GWAS initiative (1U19 CA148537, 1U19 CA148065, and 1U19 CA148112 — the GAME-ON initiative), the Department of Defence (W81XWH-10-1-0341), the Canadian Institutes of Health Research (CIHR) for the CIHR Team in Familial Risks of Breast Cancer, and Komen Foundation for the Cure, the Breast Cancer Research Foundation, and the Ovarian Cancer Research Fund. The DRIVE Consortium was funded by U19 CA148065. The Australian Breast Cancer Family Study (ABCFS) was supported by grant UM1 CA164920 from the National Cancer Institute (USA). The content of this manuscript does not necessarily re fl ect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the USA Government or the BCFR. The ABCFS was also supported by the National Health and Medical Research Council of Australia, the New South Wales Cancer Council, the Victorian Health Promotion Foundation (Aus- tralia), and the Victorian Breast Cancer Research Consortium. J.L.H. is a National Health and Medical Research Council (NHMRC) Senior Principal Research Fellow. M.C.S. is a NHMRC Senior Research Fellow. The ABCS study was supported by the Dutch Cancer Society [grants NKI 2007-3839; 2009 4363]. The Australian Breast Cancer Tissue Bank (ABCTB) is generously supported by the National Health and Medical Research Council of Australia, The Cancer Institute NSW and the National Breast Cancer Foundation. The ACP study is funded by the Breast Cancer Research Trust, UK. The AHS study is supported by the intramural research program of the National Institutes of Health, the National Cancer Institute (grant number Z01-CP010119), and the National Institute of Environmental Health Sciences (grant number Z01-ES049030). The work of the BBCC was partly funded by ELAN-Fond of the University Hospital of Erlangen. The BBCS is funded by Cancer Research UK and Breast Cancer Now and acknowledges NHS funding to the NIHR Biomedical Research Centre, and the National Cancer Research Network (NCRN). The BCEES was funded by the National Health and Medical Research Council, Australia and the Cancer Council Western Australia and acknowledges funding from the National Breast Cancer Foundation (JS). For the BCFR-NY, BCFR-PA, and BCFR-UT this work was supported by grant UM1 CA164920 from the National Cancer Institute. The content of this manuscript does not necessarily re fl ect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government or the BCFR. For BIGGS, ES is supported by NIHR Comprehensive Biomedical Research Centre, Guy ' s & St. Thomas ' NHS Foundation Trust in partnership with King ' s College London, United Kingdom. IT is supported by the Oxford Biomedical Research Centre. BOCS is supported by funds from Cancer Research UK (C8620/A8372/A15106) and the Institute of Cancer Research (UK). BOCS acknowledges NHS funding to the Royal Marsden/Institute of Cancer Research NIHR Specialist Cancer Biomedical Research Centre. The BREast Oncology GAlician Network (BREOGAN) is funded by Acción Estratégica de Salud del Instituto de Salud Carlos III FIS PI12/02125/Co fi nanciado FEDER; Acción Estratégica de Salud del Instituto de Salud Carlos III FIS Intrasalud (PI13/01136); Programa Grupos Emergentes, Cancer Genetics Unit, Instituto de Investigacion Biomedica Galicia Sur. Xerencia de Xestion Integrada de Vigo-SERGAS, Instituto de Salud Carlos III, Spain; Grant 10CSA012E, Consellería de Industria Programa Sectorial de Investigación Aplicada, PEME I + DeI + D Suma del Plan Gallego de Investigación, Desarrollo e Innovación Tecnológica de la Consellería de Industria de la Xunta de Galicia, Spain; Grant EC11-192. Fomento de la Investigación Clínica Independiente, Ministerio de Sanidad, Servicios Sociales e Igualdad, Spain; and Grant FEDER-Innterconecta. Ministerio de Economia y Competitividad, Xunta de Gali- cia, Spain. The BSUCH study was supported by the Dietmar-Hopp Foundation, the Helmholtz Society and the German Cancer Research Center (DKFZ). The CAMA study was funded by Consejo Nacional de Ciencia y Tecnología (CONACyT) (SALUD-2002- C01-7462). Sample collection and processing was funded in part by grants from the National Cancer Institute (NCI R01CA120120 and K24CA169004). CBCS is funded by the Canadian Cancer Society (grant # 313404) and the Canadian Institutes of Health Research. CCGP is supported by funding from the University of Crete. The CECILE study was supported by Fondation de France, Institut National du Cancer (INCa), Ligue Nationale contre le Cancer, Agence Nationale de Sécurité Sanitaire, de l ' Alimentation, de l ' Environnement et du Travail (ANSES), Agence Nationale de la Recherche (ANR). The CGPS was supported by the Chief Physician Johan Boserup and Lise Boserup Fund, the Danish Medical Research Council, and Herlev and Gentofte Hospital. The CNIO-BCS was supported by the Instituto de Salud Carlos III, the Red Temática de Investigación Cooperativa en Cáncer and grants from the Asociación Española Contra el Cáncer and the Fondo de Investigación Sanitario (PI11/00923 and PI12/00070). COLBCCC is sup- ported by the German Cancer Research Center (DKFZ), Heidelberg, Germany. D.T. was in part supported by a postdoctoral fellowship from the Alexander von Humboldt Foundation. The American Cancer Society funds the creation, maintenance, and updating of the CPS-II cohort. The CTS was initially supported by the California Breast Cancer Act of 1993 and the California Breast Cancer Research Fund (contract 97-10500) and is currently funded through the National Institutes of Health (R01 CA77398, UM1 CA164917, and U01 CA199277). Collection of cancer incidence data was supported by the California Department of Public Health as part of the statewide cancer reporting program mandated by California Health and Safety Code Section 103885. H.A.C eceives support from the Lon V Smith Foundation (LVS39420). The University of Westminster curates the DietCompLyf database funded by Against Breast Cancer Registered Charit.No. 1121258 and the NCRN. The coordination of EPIC is fi nancially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The national cohorts are supported by: Ligue Contre le Cancer, Institut Gustave Roussy, Mutuelle Générale de l ' Education Nationale, Institut National de la Santé et de la Recherche Médicale (INSERM) (France); German Cancer Aid, German Cancer Research Center (DKFZ), Federal Ministry of Education and Research (BMBF) (Germany); the Hellenic Health Foundation, the Stavros Niarchos Foundation (Greece); Associazione Italiana per la Ricerca sul Cancro-AIRC-Italy and National Research Council (Italy); Dutch Ministry of Public Health, Welfare and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds, Dutch Prevention Funds, Dutch ZON (Zorg Onderzoek Nederland), World Cancer Research Fund (WCRF), Statistics Netherlands (The Neth- erlands); Health Research Fund (FIS), PI13/00061 to Granada, PI13/01162 to EPIC- Murcia, Regional Governments of Andalucía, Asturias, Basque Country, Murcia and Navarra, ISCIII RETIC (RD06/0020) (Spain); Cancer Research UK (14136 to EPIC- Norfolk; C570/A16491 and C8221/A19170 to EPIC-Oxford), Medical Research Council (1000143 to EPIC-Norfolk, MR/M012190/1 to EPIC-Oxford) (United Kingdom). The ESTHER study was supported by a grant from the Baden Württemberg Ministry of Science, Research and Arts. Additional cases were recruited in the context of the VERDI study, which was supported by a grant from the German Cancer Aid (Deutsche Kreb- shilfe). FHRISK is funded from NIHR grant PGfAR 0707-10031. The GC-HBOC (Ger- man Consortium of Hereditary Breast and Ovarian Cancer) is supported by the German Cancer Aid (grant no 110837, coordinator: Rita K. Schmutzler, Cologne). This work was also funded by the European Regional Development Fund and Free State of Saxony, Germany (LIFE - Leipzig Research Centre for Civilization Diseases, project numbers 713- 241202, 713-241202, 14505/2470, and 14575/2470). The GENICA was funded by the Federal Ministry of Education and Research (BMBF) Germany grants 01KW9975/5, 01KW9976/8, 01KW9977/0, and 01KW0114, the Robert Bosch Foundation, Stuttgart, Deutsches Krebsforschungszentrum (DKFZ), Heidelberg, the Institute for Prevention and Occupational Medicine of the German Social Accident Insurance, Institute of the Ruhr University Bochum (IPA), Bochum, as well as the Department of Internal Medicine, Evangelische Kliniken Bonn gGmbH, Johanniter Krankenhaus, Bonn, Germany. The GEPARSIXTO study was conducted by the German Breast Group GmbH. The GESBC was supported by the Deutsche Krebshilfe e. V. [70492] and the German Cancer Research Center (DKFZ). GLACIER was supported by Breast Cancer Now, CRUK and Biomedical Research Centre at Guy ' s and St Thomas ' NHS Foundation Trust and King ' s College London. The HABCS study was supported by the Claudia von Schilling Foundation for Breast Cancer Research, by the Lower Saxonian Cancer Society, and by the Rudolf- Bartling Foundation. The HEBCS was fi nancially supported by the Helsinki University Central Hospital Research Fund, Academy of Finland (266528), the Finnish Cancer Society, and the Sigrid Juselius Foundation. The HERPACC was supported by MEXT Kakenhi (No. 170150181 and 26253041) from the Ministry of Education, Science, Sports, Culture and Technology of Japan, by a Grant-in-Aid for the Third Term Comprehensive 10-Year Strategy for Cancer Control from Ministry Health, Labour and Welfare of Japan, by Health and Labour Sciences Research Grants for Research on Applying Health Technology from Ministry Health, Labour and Welfare of Japan, by National Cancer Center Research and Development Fund, and " Practical Research for Innovative Cancer Control (15ck0106177h0001) " from Japan Agency for Medical Research and develop- ment, AMED, and Cancer Bio Bank Aichi. The HMBCS was supported by a grant from the Friends of Hannover Medical School and by the Rudolf Bartling Foundation. The HUBCS was supported by a grant from the German Federal Ministry of Research and Education (RUS08/017), and by the Russian Foundation for Basic Research and the Federal Agency for Scienti fi c Organizations for support the Bioresource collections and RFBR grants 14-04-97088, 17-29-06014, and 17-44-020498. ICICLE was supported by Breast Cancer Now, CRUK, and Biomedical Research Centre at Guy ' s and St Thomas ' NHS Foundation Trust and King ' s College London. Financial support for KARBAC was provided through the regional agreement on medical training and clinical research (A.L. F.) between Stockholm County Council and Karolinska Institutet, the Swedish Cancer Society, The Gustav V Jubilee foundation and Bert von Kantzows foundation. The KARMA study was supported by Märit and Hans Rausings Initiative Against Breast Cancer. The KBCP was fi nancially supported by the special Government Funding (E.V. O.) of Kuopio University Hospital grants, Cancer Fund of North Savo, the Finnish Cancer Organizations, and by the strategic funding of the University of Eastern Finland. kConFab is supported by a grant from the National Breast Cancer Foundation, and previously by the National Health and Medical Research Council (NHMRC), the Queensland Cancer Fund, the Cancer Councils of New South Wales, Victoria, Tasmania and South Australia, and the Cancer Foundation of Western Australia. Financial support for the AOCS was provided by the United States Army Medical Research and Materiel Command [DAMD17-01-1-0729], Cancer Council Victoria, Queensland Cancer Fund, Cancer Council New South Wales, Cancer Council South Australia, The Cancer Foundation of Western Australia, Cancer Council Tasmania and the National Health and Medical Research Council of Australia (NHMRC; 400413, 400281, 199600). G.C.-T. and P.W. are supported by the NHMRC. RB was a Cancer Institute NSW Clinical Research Fellow. The KOHBRA study was partially supported by a grant from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), and the National R&D Program for Cancer Control, Ministry of Health & Welfare, Republic of Korea (HI16C1127; 1020350; 1420190). LAABC is supported by grants (1RB-0287, 3PB- 0102, 5PB-0018, 10PB-0098) from the California Breast Cancer Research Program. Incident breast cancer cases were collected by the USC Cancer Surveillance Program (CSP) which is supported under subcontract by the California Department of Health. TheCSP is also part of the National Cancer Institute ' s Division of Cancer Prevention and Control Surveillance, Epidemiology, and End Results Program, under contract number N01CN25403. L.M.B.C. is supported by the ' Stichting tegen Kanker ' . D.L. is supported by the FWO. The MABCS study is funded by the Research Centre for Genetic Engineering and Biotechnology " Georgi D. Efremov " and supported by the German Academic Exchange Program, DAAD. The MARIE study was supported by the Deutsche Krebshilfe e.V. [70-2892-BR I, 106332, 108253, 108419, 110826, 110828], the Hamburg Cancer Society, the German Cancer Research Center (DKFZ) and the Federal Ministry of Edu- cation and Research (BMBF) Germany [01KH0402]. MBCSG is supported by grants from the Italian Association for Cancer Research (AIRC) and by funds from the Italian citizens who allocated the 5/1000 share of their tax payment in support of the Fondazione IRCCS Istituto Nazionale Tumori, according to Italian laws (INT-Institutional strategic projects " 5 × 1000 " ). The MCBCS was supported by the NIH grants CA192393, CA116167, CA176785 an NIH Specialized Program of Research Excellence (SPORE) in Breast Cancer [CA116201], and the Breast Cancer Research Foundation and a generous gift from the David F. and Margaret T. Grohne Family Foundation. MCCS cohort recruitment was funded by VicHealth and Cancer Council Victoria. The MCCS was further supported by Australian NHMRC grants 209057 and 396414, and by infrastructure provided by Cancer Council Victoria. Cases and their vital status were ascertained through the Victorian Cancer Registry (VCR) and the Australian Institute of Health and Welfare (AIHW), including the National Death Index and the Australian Cancer Database. The MEC was support by NIH grants CA63464, CA54281, CA098758, CA132839, and CA164973. The MISS study is supported by funding from ERC-2011-294576 Advanced grant, Swedish Cancer Society, Swedish Research Council, Local hospital funds, Berta Kamprad Foun- dation, Gunnar Nilsson. The MMHS study was supported by NIH grants CA97396, CA128931, CA116201, CA140286, and CA177150. MSKCC is supported by grants from the Breast Cancer Research Foundation and Robert and Kate Niehaus Clinical Cancer Genetics Initiative. The work of MTLGEBCS was supported by the Quebec Breast Cancer Foundation, the Canadian Institutes of Health Research for the " CIHR Team in Familial Risks of Breast Cancer " program – grant # CRN-87521 and the Ministry of Economic Development, Innovation and Export Trade – grant # PSR-SIIRI-701. MYBRCA is funded by research grants from the Malaysian Ministry of Higher Education (UM.C/HlR/MOHE/ 06) and Cancer Research Malaysia. MYMAMMO is supported by research grants from Yayasan Sime Darby LPGA Tournament and Malaysian Ministry of Higher Education (RP046B-15HTM). The NBCS has been supported by the Research Council of Norway grant 193387/V50 (to A.-L. Børresen-Dale and V.N. Kristensen) and grant 193387/H10 (to A.-L. Børresen-Dale and V.N. Kristensen), South Eastern Norway Health Authority (grant 39346 to A.-L. Børresen-Dale and 27208 to V.N. Kristensen) and the Norwegian Cancer Society (to A.-L. Børresen-Dale and 419616 - 71248 - PR-2006-0282 to V.N. Kristensen). It has received funding from the K.G. Jebsen Centre for Breast Cancer Research (2012-2015). The NBHS was supported by NIH grant R01CA100374. Biological sample preparation was conducted the Survey and Biospecimen Shared Resource, which is supported by P30 CA68485. The Northern California Breast Cancer Family Registry (NC- BCFR) and Ontario Familial Breast Cancer Registry (OFBCR) were supported by grant UM1 CA164920 from the National Cancer Institute (USA). The content of this manu- script does not necessarily re fl ect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the USA Government or the BCFR. The Carolina Breast Cancer Study was funded by Komen Foundation, the National Cancer Institute (P50 CA058223, U54 CA156733, and U01 CA179715), and the North Carolina University Cancer Research Fund. The NGOBCS was supported by Grants-in-Aid for the Third Term Comprehensive Ten-Year Strategy for Cancer Control from the Ministry of Health, Labor and Welfare of Japan, and for Scienti fi c Research on Priority Areas, 17015049 and for Scienti fi c Research on Innovative Areas, 221S0001, from the Ministry of Education, Culture, Sports, Science, and Technology of Japan. The NHS was supported by NIH grants P01 CA87969, UM1 CA186107, and U19 CA148065. The NHS2 was supported by NIH grants UM1 CA176726 and U19 CA148065. The OBCS was supported by research grants from the Finnish Cancer Foundation, the Academy of Finland (grant number 250083, 122715 and Center of Excellence grant number 251314), the Finnish Cancer Foundation, the Sigrid Juselius Foundation, the University of Oulu, the University of Oulu Support Foundation, and the special Governmental EVO funds for Oulu University Hospital-based research activities. The ORIGO study was supported by the Dutch Cancer Society (RUL 1997- 1505) and the Biobanking and Biomolecular Resources Research Infrastructure (BBMRI- NL CP16). The PBCS was funded by Intramural Research Funds of the National Cancer Institute, Department of Health and Human Services, USA. Genotyping for PLCO was supported by the Intramural Research Program of the National Institutes of Health, NCI, Division of Cancer Epidemiology and Genetics. The PLCO is supported by the Intramural Research Program of the Division of Cancer Epidemiology and Genetics and supported by contracts from the Division of Cancer Prevention, National Cancer Institute, National Institutes of Health. The POSH study is funded by Cancer Research UK (grants C1275/ A11699, C1275/C22524, C1275/A19187, C1275/A15956, and Breast Cancer Campaign 2010PR62, 2013PR044. PROCAS is funded from NIHR grant PGfAR 0707-10031. The RBCS was funded by the Dutch Cancer Society (DDHK 2004-3124, DDHK 2009-4318). The SASBAC study was supported by funding from the Agency for Science, Technology and Research of Singapore (A*STAR), the US National Institute of Health (NIH) and the Susan G. Komen Breast Cancer Foundation. The SBCGS was supported primarily by NIH grants R01CA64277, R01CA148667, UMCA182910, and R37CA70867. Biological sample preparation was conducted the Survey and Biospecimen Shared Resource, which is supported by P30 CA68485. The scienti fi c development and funding of this project were, in part, supported by the Genetic Associations and Mechanisms in Oncology (GAME- ON) Network U19 CA148065. The SBCS was supported by Shef fi eld Experimental Cancer Medicine Centre and Breast Cancer Now Tissue Bank. The SCCS is supported by a grant from the National Institutes of Health (R01 CA092447). Data on SCCS cancer cases used in this publication were provided by the Alabama Statewide Cancer Registry; Kentucky Cancer Registry, Lexington, KY; Tennessee Department of Health, Of fi ce of Cancer Surveillance; Florida Cancer Data System; North Carolina Central Cancer Registry, North Carolina Division of Public Health; Georgia Comprehensive Cancer Registry; Louisiana Tumor Registry; Mississippi Cancer Registry; South Carolina Central Cancer Registry; Virginia Department of Health, Virginia Cancer Registry; Arkansas Department of Health, Cancer Registry, 4815 W. Markham, Little Rock, AR 72205. The Arkansas Central Cancer Registry is fully funded by a grant from National Program of Cancer Registries, Centers for Disease Control and Prevention (CDC). Data on SCCS cancer cases from Mississippi were collected by the Mississippi Cancer Registry which participates in the National Program of Cancer Registries (NPCR) of the Centers for Disease Control and Prevention (CDC). The contents of this publication are solely the responsibility of the authors and do not necessarily represent the of fi cial views of the CDC or the Mississippi Cancer Registry. SEARCH is funded by Cancer Research UK [C490/A10124, C490/ A16561] and supported by the UK National Institute for Health Research Biomedical Research Centre at the University of Cambridge. The University of Cambridge has received salary support for PDPP from the NHS in the East of England through the Clinical Academic Reserve. SEBCS was supported by the BRL (Basic Research Laboratory) program through the National Research Foundation of Korea funded by the Ministry of Education, Science and Technology (2012-0000347). SGBCC is funded by the NUS start- up Grant, National University Cancer Institute Singapore (NCIS) Centre Grant and the NMRC Clinician Scientist Award. Additional controls were recruited by the Singapore Consortium of Cohort Studies-Multi-ethnic cohort (SCCS-MEC), which was funded by the Biomedical Research Council, grant number: 05/1/21/19/425. The Sister Study (SIS- TER) is supported by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences (Z01-ES044005 and Z01-ES049033). The Two Sister Study (2SISTER) was supported by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences (Z01-ES044005 and Z01-ES102245), and, also by a grant from Susan G. Komen for the Cure, grant FAS0703856. SKKDKFZS is supported by the DKFZ. The SMC is funded by the Swedish Cancer Foundation. The SZBCS was supported by Grant PBZ_KBN_122/P05/2004. The TBCS was funded by The National Cancer Institute, Thailand. The TNBCC was supported by a Specialized Program of Research Excellence (SPORE) in Breast Cancer (CA116201), a grant from the Breast Cancer Research Foundation, a generous gift from the David F. and Margaret T. Grohne Family Foundation. The TWBCS is supported by the Taiwan Biobank project of the Institute of Biomedical Sciences, Academia Sinica, Taiwan. The UCIBCS component of this research was supported by the NIH [CA58860, CA92044] and the Lon V Smith Foundation [LVS39420]. The UKBGS is funded by Breast Cancer Now and the Institute of Cancer Research (ICR), London. ICR acknowledges NHS funding to the NIHR Bio- medical Research Centre. The UKOPS study was funded by The Eve Appeal (The Oak Foundation) and supported by the National Institute for Health Research University College London Hospitals Biomedical Research Centre. The US3SS study was supported by Massachusetts (K.M.E., R01CA47305), Wisconsin (P.A.N., R01 CA47147) and New Hampshire (L.T.-E., R01CA69664) centers, and Intramural Research Funds of the National Cancer Institute, Department of Health and Human Services, USA. The USRT Study was funded by Intramural Research Funds of the National Cancer Institute, Department of Health and Human Services, USA. The WAABCS study was supported by grants from the National Cancer Institute of the National Institutes of Health (R01 CA89085 and P50 CA125183 and the D43 TW009112 grant), Susan G. Komen (SAC110026), the Dr. Ralph and Marian Falk Medical Research Trust, and the Avon Foundation for Women. The WHI program is funded by the National Heart, Lung, and Blood Institute, the US National Institutes of Health and the US Department of Health and Human Services (HHSN268201100046C, HHSN268201100001C, HHSN268201100002C, HHSN268201100003C, HHSN268201100004C, and HHSN271201100004C). This work was also funded by NCI U19 CA148065-01. D.G.E. is supported by the all Manchester NIHR Biomedical research center Manchester (IS-BRC- 1215-20007). HUNBOCS, Hungarian Breast and Ovarian Cancer Study was supported by Hungarian Research Grant KTIA-OTKA CK-80745, NKFI_OTKA K-112228. C.I. received support from the Nontherapeutic Subject Registry Shared Resource at George- town University (NIH/NCI P30-CA-51008) and the Jess and Mildred Fisher Center for Hereditary Cancer and Clinical Genomics Research. K.M. is supported by CRUK C18281/ A19169. City of Hope Clinical Cancer Community Research Network and the Hereditary Cancer Research Registry, supported in part by Award Number RC4CA153828 (PI: J Weitzel) from the National Cancer Institute and the of fi ce of the Directory, National Institutes of Health. The content is solely the responsibility of the authors and does not necessarily represent the of fi cial views of the National Institutes of Health. The colorectal cancer genome-wide association analyses: Colorectal Transdisciplinary Study (CORECT): The content of this manuscript does not necessarily re fl ect the views or policies of the National Cancer Institute or any of the collaborating centers in the CORECT Consortium, nor does mention of trade names, commercial products or organizations imply endor- sement by the US Government or the CORECT Consortium. We are incredibly grateful for the contributions of Dr. Brian Henderson and Dr. Roger Green over the course of this study and acknowledge them in memoriam. We are also grateful for support from Daniel and Maryann Fong. ColoCare: we thank the many investigators and staff who made thisHHSN268201600001C, HHSN268201600002C, HHSN268201600003C, and HHSN26 8201600004C. The head and neck cancer genome-wide association analyses: The study was supported by NIH/NCI: P50 CA097190, and P30 CA047904, Canadian Cancer Society Research Institute (no. 020214) and Cancer Care Ontario Research Chair to R.H. The Princess Margaret Hospital Head and Neck Cancer Translational Research Program is funded by the Wharton family, Joe ' s Team, Gordon Tozer, Bruce Galloway and the Elia family. Geoffrey Liu was supported by the Posluns Family Fund and the Lusi Wong Family Fund at the Princess Margaret Foundation, and the Alan B. Brown Chair in Molecular Genomics. This publication presents data from Head and Neck 5000 (H&N5000). H&N5000 was a component of independent research funded by the UK National Institute for Health Research (NIHR) under its Programme Grants for Applied Research scheme (RP-PG-0707-10034). The views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health. Human papillomavirus (HPV) in H&N5000 serology was supported by a Cancer Research UK Programme Grant, the Integrative Cancer Epidemiology Programme (grant number: C18281/A19169). National Cancer Institute (R01-CA90731); National Institute of Environmental Health Sciences (P30ES10126). The authors thank all the members of the GENCAPO team/The Head and Neck Genome Project (GENCAPO) was supported by the Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) (Grant numbers 04/12054-9 and 10/51168-0). CPS-II recruitment and maintenance is supported with intramural research funding from the American Cancer Society. Genotyping per- formed at the Center for Inherited Disease Research (CIDR) was funded through the U.S. National Institute of Dental and Craniofacial Research (NIDCR) grant 1 × 01HG007780- 0. The University of Pittsburgh head and neck cancer case-control study is supported by National Institutes of Health grants P50 CA097190 and P30 CA047904. The Carolina Head and Neck Cancer Study (CHANCE) was supported by the National Cancer Institute (R01-CA90731). The Head and Neck Genome Project (GENCAPO) was supported by the Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) (Grant numbers 04/ 12054-9 and 10/51168-0). The authors thank all the members of the GENCAPO team. The HN5000 study was funded by the National Institute for Health Research (NIHR) under its Programme Grants for Applied Research scheme (RP-PG-0707-10034), the views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health. The Toronto study was funded by the Canadian Cancer Society Research Institute (020214) and the National Cancer Institute (U19-CA148127) and the Cancer Care Ontario Research Chair. The alcohol-related cancers and genetic susceptibility study in Europe (ARCAGE) was funded by the Eur- opean Commission ' s 5th Framework Program (QLK1-2001-00182), the Italian Associa- tion for Cancer Research, Compagnia di San Paolo/FIRMS, Region Piemonte, and Padova University (CPDA057222). The Rome Study was supported by the Associazione Italiana per la Ricerca sul Cancro (AIRC) IG 2011 10491 and IG2013 14220 to S.B., and Fon- dazione Veronesi to S.B. The IARC Latin American study was funded by the European Commission INCO-DC programme (IC18-CT97-0222), with additional funding from Fondo para la Investigacion Cienti fi ca y Tecnologica (Argentina) and the Fundação de Amparo à Pesquisa do Estado de São Paulo (01/01768-2). We thank Leticia Fernandez, Instituto Nacional de Oncologia y Radiobiologia, La Habana, Cuba and Sergio and Rosalina Koifman, for their efforts with the IARC Latin America study São Paulo center. The IARC Central Europe study was supported by European Commission ' s INCO- COPERNICUS Program (IC15- CT98-0332), NIH/National Cancer Institute grant CA92039, and the World Cancer Research Foundation grant WCRF 99A28. The IARC Oral Cancer Multicenter study was funded by grant S06 96 202489 05F02 from Europe against Cancer; grants FIS 97/0024, FIS 97/0662, and BAE 01/5013 from Fondo de Investigaciones Sanitarias, Spain; the UICC Yamagiwa-Yoshida Memorial International Cancer Study; the National Cancer Institute of Canada; Associazione Italiana per la Ricerca sul Cancro; and the Pan-American Health Organization. Coordination of the EPIC study is fi nancially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The lung cancer genome-wide association analyses: Transdisciplinary Research for Cancer in Lung (TRICL) of the International Lung Cancer Consortium (ILCCO) was supported by (U19-CA148127, CA148127S1, U19CA203654, and Cancer Prevention Research Institute of Texas RR170048). The ILCCO data harmonization is supported by Cancer Care Ontario Research Chair of Population Studies to R. H. and Lunenfeld-Tanenbaum Research Institute, Sinai Health System. The TRICL-ILCCO OncoArray was supported by in-kind genotyping by the Centre for Inherited Disease Research (26820120008i-0-26800068-1). The CAPUA study was supported by FIS-FEDER/Spain grant numbers FIS-01/310, FIS-PI03-0365, and FIS- 07-BI060604, FICYT/Asturias grant numbers FICYT PB02-67 and FICYT IB09-133, and the University Institute of Oncology (IUOPA), of the University of Oviedo and the Ciber de Epidemiologia y Salud Pública. CIBERESP, SPAIN. The work performed in the CARET study was supported by the National Institute of Health/National Cancer Insti- tute: UM1 CA167462 (PI: Goodman), National Institute of Health UO1-CA6367307 (PIs Omen, Goodman); National Institute of Health R01 CA111703 (PI Chen), National Institute of Health 5R01 CA151989-01A1(PI Doherty). The Liverpool Lung project is supported by the Roy Castle Lung Cancer Foundation. The Harvard Lung Cancer Study was supported by the NIH (National Cancer Institute) grants CA092824, CA090578, CA074386. The Multi-ethnic Cohort Study was partially supported by NIH Grants CA164973, CA033619, CA63464, and CA148127. The work performed in MSH-PMH study was supported by The Canadian Cancer Society Research Institute (020214), Ontario Institute of Cancer and Cancer Care Ontario Chair Award to R.J.H. and G.L. and the Alan Brown Chair and Lusi Wong Programs at the Princess Margaret Hospital Foundation. NJLCS was funded by the State Key Program of National Natural Science ofChina (81230067), the National Key Basic Research Program Grant (2011CB503805), the Major Program of the National Natural Science Foundation of China (81390543). The Norway study was supported by Norwegian Cancer Society, Norwegian Research Council. The Shanghai Cohort Study (SCS) was supported by National Institutes of Health R01 CA144034 (PI: Yuan) and UM1 CA182876 (PI: Yuan). The Singapore Chinese Health Study (SCHS) was supported by National Institutes of Health R01 CA144034 (PI: Yuan) and UM1 CA182876 (PI: Yuan). The work in TLC study has been supported in part the James & Esther King Biomedical Research Program (09KN-15), National Institutes of Health Specialized Programs of Research Excellence (SPORE) Grant (P50 CA119997), and by a Cancer Center Support Grant (CCSG) at the H. Lee Mof fi tt Cancer Center and Research Institute, an NCI designated Comprehensive Cancer Center (grant number P30- CA76292). The Vanderbilt Lung Cancer Study — BioVU dataset used for the analyses described was obtained from Vanderbilt University Medical Center ' s BioVU, which is supported by institutional funding, the 1S10RR025141-01 instrumentation award, and by the Vanderbilt CTSA grant UL1TR000445 from NCATS/NIH. Dr. Aldrich was supported by NIH/National Cancer Institute K07CA172294 (PI: Aldrich) and Dr. Bush was sup- ported by NHGRI/NIH U01HG004798 (PI: Crawford). The Copenhagen General Population Study (CGPS) was supported by the Chief Physician Johan Boserup and Lise Boserup Fund, the Danish Medical Research Council and Herlev Hospital. The NELCS study: Grant Number P20RR018787 from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH). The Kentucky Lung Cancer Research Initiative was supported by the Department of Defense [Congressionally Directed Medical Research Program, U.S. Army Medical Research and Materiel Com- mand Program] under award number: 10153006 (W81XWH-11-1-0781). Views and opinions of, and endorsements by the author(s) do not re fl ect those of the US Army or the Department of Defense. This research was also supported by unrestricted infrastructure funds from the UK Center for Clinical and Translational Science, NIH grant UL1TR000117 and Markey Cancer Center NCI Cancer Center Support Grant (P30 CA177558) Shared Resource Facilities: Cancer Research Informatics, Biospecimen and Tissue Procurement, and Biostatistics and Bioinformatics. The M.D. Anderson Cancer Center study was supported in part by grants from the NIH (P50 CA070907, R01 CA176568) (to X.W.), Cancer Prevention & Research Institute of Texas (RP130502) (to X. W.), and The University of Texas MD Anderson Cancer Center institutional support for the Center for Translational and Public Health Genomics. The deCODE study of smoking and nicotine dependence was funded in part by a grant from NIDA (R01- DA017932). The study in Lodz center was partially funded by Nofer Institute of Occupational Med- icine, under task NIOM 10.13: Predictors of mortality from non-small cell lung cancer — fi eld study. Genetic sharing analysis was funded by NIH grant CA194393. The research undertaken by M.D.T., L.V.W., and M.S.A. was partly funded by the National Institute for Health Research (NIHR). The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health. M.D.T. holds a Medical Research Council Senior Clinical Fellowship (G0902313). The work to assemble the FTND GWAS meta-analysis was supported by the National Institutes of Health (NIH), National Institute on Drug Abuse (NIDA) grant number R01 DA035825 (Prin- cipal Investigator [PI]: DBH). The study populations included COGEND (dbGaP phs000092.v1.p1 and phs000404.v1.p1), COPDGene (dbGaP phs000179.v3.p2), deCODE Genetics, EAGLE (dbGaP phs000093.vs.p2), and SAGE. dbGaP phs000092.v1.p1). See Hancock et al. Transl Psychiatry 2015 (PMCID: PMC4930126) for the full listing of funding sources and other acknowledgments. The Resource for the Study of Lung Cancer Epidemiology in North Trent (ReSoLuCENT)study was funded by the Shef fi eld Hospitals Charity, Shef fi eld Experimental Cancer Medicine Centre and Weston Park Hospital Cancer Charity. The ovarian cancer genome-wide association analysis: The Ovarian Cancer Association Consortium (OCAC) is supported by a grant from the Ovarian Cancer Research Fund thanks to donations by the family and friends of Kathryn Sladek Smith (PPD/RPCI.07). The scienti fi c development and funding for this project were in part supported by the US National Cancer Institute GAME-ON Post-GWAS Initiative (U19-CA148112). This study made use of data generated by the Wellcome Trust Case Control consortium that was funded by the Wellcome Trust under award 076113. The results published here are in part based upon data generated by The Cancer Genome Atlas Pilot Project established by the National Cancer Institute and National Human Genome Research Institute (dbGap accession number phs000178.v8.p7). The OCAC OncoArray genotyping project was funded through grants from the U.S. National Institutes of Health (CA1X01HG007491-01 (C.I.A.), U19-CA148112 (T.A.S.), R01-CA149429 (C.M.P.), and R01-CA058598 (M.T.G.); Canadian Institutes of Health Research (MOP-86727 (L.E.K.) and the Ovarian Cancer Research Fund (A.B.). The COGS project was funded through a European Commission ' s Seventh Framework Programme grant (agreement number 223175 - HEALTH-F2-2009-223175) and through a grant from the U.S. National Insti- tutes of Health (R01-CA122443 (E.L.G)). Funding for individual studies: AAS: National Institutes of Health (RO1-CA142081); AOV: The Canadian Institutes for Health Research (MOP-86727); AUS: The Australian Ovarian Cancer Study Group was supported by the U.S. Army Medical Research and Materiel Command (DAMD17-01-1-0729), National Health & Medical Research Council of Australia (199600, 400413 and 400281), Cancer Councils of New South Wales, Victoria, Queensland, South Australia and Tas- mania and Cancer Foundation of Western Australia (Multi-State Applications 191, 211, and 182). The Australian Ovarian Cancer Study gratefully acknowledges additional support from Ovarian Cancer Australia and the Peter MacCallum Foundation; BAV: ELAN Funds of the University of Erlangen-Nuremberg; BEL: National Kankerplan; BGS: Breast Cancer Now, Institute of Cancer Research; BVU: Vanderbilt CTSA grant from the National Institutes of Health (NIH)/National Center for Advancing Translational SciencesNCATS) (ULTR000445); CAM: National Institutes of Health Research Cambridge Biomedical Research Centre and Cancer Research UK Cambridge Cancer Centre; CHA: Innovative Research Team in University (PCSIRT) in China (IRT1076); CNI: Instituto de Salud Carlos III (PI12/01319); Ministerio de Economía y Competitividad (SAF2012); COE: Department of Defense (W81XWH-11-2-0131); CON: National Institutes of Health (R01-CA063678, R01-CA074850; and R01-CA080742); DKE: Ovarian Cancer Research Fund; DOV: National Institutes of Health R01-CA112523 and R01-CA87538; EMC: Dutch Cancer Society (EMC 2014-6699); EPC: The coordination of EPIC is fi nancially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The national cohorts are supported by Danish Cancer Society (Denmark); Ligue Contre le Cancer, Institut Gustave Roussy, Mutuelle Générale de l ' Education Nationale, Institut National de la Santé et de la Recherche Médicale (INSERM) (France); German Cancer Aid, German Cancer Research Center (DKFZ), Federal Ministry of Education and Research (BMBF) (Germany); the Hellenic Health Foundation (Greece); Associazione Italiana per la Ricerca sul Cancro-AIRC-Italy and National Research Council (Italy); Dutch Ministry of Public Health, Welfare and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds, Dutch Prevention Funds, Dutch ZON (Zorg Onderzoek Nederland), World Cancer Research Fund (WCRF), Statistics Netherlands (The Netherlands); ERC-2009-AdG 232997 and Nordforsk, Nordic Centre of Excellence programme on Food, Nutrition and Health (Norway); Health Research Fund (FIS), PI13/00061 to Granada, PI13/01162 to EPIC-Murcia, Regional Governments of Andalucía, Asturias, Basque Country, Murcia and Navarra, ISCIII RETIC (RD06/0020) (Spain); Swedish Cancer Society, Swedish Research Council and County Councils of Skåne and Västerbotten (Sweden); Cancer Research UK (14136 to EPIC- Norfolk; C570/A16491 and C8221/A19170 to EPIC-Oxford), Medical Research Council (1000143 to EPIC-Norfolk, MR/M012190/1 to EPIC-Oxford) (United Kingdom); GER: German Federal Ministry of Education and Research, Programme of Clinical Biomedical Research (01 GB 9401) and the German Cancer Research Center (DKFZ); GRC: This research has been co- fi nanced by the European Union (European Social Fund — ESF) and Greek national funds through the Operational Program " Education and Lifelong Learn- ing " of the National Strategic Reference Framework (NSRF) — Research Funding Program of the General Secretariat for Research & Technology: SYN11_10_19 NBCA. Investing in knowledge society through the European Social Fund; GRR: Roswell Park Cancer Institute Alliance Foundation, P30 CA016056; HAW: U.S. National Institutes of Health (R01- CA58598, N01-CN-55424, and N01-PC-67001); HJO: Intramural funding; Rudolf- Bartling Foundation; HMO: Intramural funding; Rudolf-Bartling Foundation; HOC: Helsinki University Research Fund; HOP: Department of Defense (DAMD17-02-1-0669) and NCI (K07-CA080668, R01-CA95023, P50-CA159981 MO1-RR000056 R01- CA126841); HUO: Intramural funding; Rudolf-Bartling Foundation; JGO: JSPS KAKENHI grant; JPN: Grant-in-Aid for the Third Term Comprehensive 10-Year Strategy for Cancer Control from the Ministry of Health, Labour and Welfare; KRA: This study (Ko-EVE) was supported by a grant from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), and the National R&D Program for Cancer Control, Ministry of Health & Welfare, Republic of Korea (HI16C1127; 0920010); LAX: American Cancer Society Early Detection Professorship (SIOP-06-258-01-COUN) and the National Center for Advancing Translational Sciences (NCATS), Grant UL1TR000124; LUN: ERC-2011-AdG 294576-risk factors cancer, Swedish Cancer Society, Swedish Research Council, Beta Kamprad Foundation; MAC: National Institutes of Health (R01-CA122443, P30-CA15083, P50-CA136393); Mayo Foundation; Minnesota Ovarian Cancer Alliance; Fred C. and Katherine B. Andersen Foundation; Fraternal Order of Eagles; MAL: Funding for this study was provided by research grant R01- CA61107 from the National Cancer Institute, Bethesda, MD, research grant 94 222 52 from the Danish Cancer Society, Copenhagen, Denmark; and the Mer- maid I project; MAS: Malaysian Ministry of Higher Education (UM.C/HlR/MOHE/06) and Cancer Research Initiatives Foundation; MAY: National Institutes of Health (R01- CA122443, P30-CA15083, and P50-CA136393); Mayo Foundation; Minnesota Ovarian Cancer Alliance; Fred C. and Katherine B. Andersen Foundation; MCC: Cancer Council Victoria, National Health and Medical Research Council of Australia (NHMRC) grants number 209057, 251533, 396414, and 504715; MDA: DOD Ovarian Cancer Research Program (W81XWH-07-0449); MEC: NIH (CA54281, CA164973, CA63464); MOF: Mof fi tt Cancer Center, Merck Pharmaceuticals, the state of Florida, Hillsborough County, and the city of Tampa; NCO: National Institutes of Health (R01-CA76016) and the Department of Defense (DAMD17-02-1-0666); NEC: National Institutes of Health R01- CA54419 and P50-CA105009 and Department of Defense W81XWH-10-1-02802; NHS: UM1 CA186107, P01 CA87969, R01 CA49449, R01-CA67262, UM1 CA176726; NJO: National Cancer Institute (NIH-K07 CA095666, R01-CA83918, NIH-K22-CA138563, and P30-CA072720) and the Cancer Institute of New Jersey; If Sara Olson and/or Irene Orlow is a co-author, please add NCI CCSG award (P30-CA008748) to the funding sources; NOR: Helse Vest, The Norwegian Cancer Society, The Research Council of Norway; NTH: Radboud University Medical Centre; OPL: National Health and Medical Research Council (NHMRC) of Australia (APP1025142) and Brisbane Women ' s Club; ORE: OHSU Foundation; OVA: This work was supported by Canadian Institutes of Health Research grant (MOP-86727) and by NIH/NCI 1 R01CA160669-01A1; PLC: Intramural Research Program of the National Cancer Institute; POC: Pomeranian Medical Uni- versity; POL: Intramural Research Program of the National Cancer Institute; PVD: Canadian Cancer Society and Cancer Research Society GRePEC Program; RBH: National Health and Medical Research Council of Australia; RMH: Cancer Research UK, Royal Marsden Hospital; RPC: National Institute of Health (P50-CA159981, R01-CA126841); SEA: Cancer Research UK (C490/A10119 C490/A10124); UK National Institute forHealth Research Biomedical Research Centres at the University of Cambridge; SIS: NIH, National Institute of Environmental Health Sciences, Z01-ES044005 and Z01-ES049033; SMC: The bbSwedish Research Council-SIMPLER infrastructure; the Swedish Cancer Foundation; SON: National Health Research and Development Program, Health Canada, grant 6613-1415-53; SRO: Cancer Research UK (C536/A13086, C536/A6689) and Imperial Experimental Cancer Research Centre (C1312/A15589); STA: NIH grants U01 CA71966 and U01 CA69417; SWE: Swedish Cancer foundation, WeCanCureCancer and VårKampMotCancer foundation; SWH: NIH (NCI) grant R37-CA070867; TBO: National Institutes of Health (R01-CA106414-A2), American Cancer Society (CRTG-00-196-01- CCE), Department of Defense (DAMD17-98-1-8659), Celma Mastery Ovarian Cancer Foundation; TOR: NIH grants R01-CA063678 and R01 CA063682; UCI: NIH R01- CA058860 and the Lon V Smith Foundation grant LVS39420; UHN: Princess Margaret Cancer Centre Foundation-Bridge for the Cure; UKO: The UKOPS study was funded by The Eve Appeal (The Oak Foundation) and supported by the National Institute for Health Research University College London Hospitals Biomedical Research Centre; UKR: Cancer Research UK (C490/A6187), UK National Institute for Health Research Biomedical Research Centres at the University of Cambridge; USC: P01CA17054, P30CA14089, R01CA61132, N01PC67010, R03CA113148, R03CA115195, N01CN025403, and Cali- fornia Cancer Research Program (00-01389V-20170, 2II0200); VAN: BC Cancer Foun- dation, VGH & UBC Hospital Foundation; VTL: NIH K05-CA154337; WMH: National Health and Medical Research Council of Australia, Enabling Grants ID 310670 & ID 628903. Cancer Institute NSW Grants 12/RIG/1-17 & 15/RIG/1-16; WOC: National Science Centren (N N301 5645 40). The Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Warsaw, Poland. The University of Cambridge has received salary support for PDPP from the NHS in the East of England through the Clinical Academia Reserve. The prostate cancer genome-wide association analyses: we pay tribute to Brian Henderson, who was a driving force behind the OncoArray project, for his vision and leadership, and who sadly passed away before seeing its fruition. We also thank the individuals who participated in these studies enabling this work. The ELLIPSE/ PRACTICAL (http//:practical.icr.ac.uk) prostate cancer consortium and his collaborating partners were supported by multiple funding mechanisms enabling this current work. ELLIPSE/PRACTICAL Genotyping of the OncoArray was funded by the US National Institutes of Health (NIH) (U19 CA148537 for ELucidating Loci Involved in Prostate Cancer SuscEptibility (ELLIPSE) project and X01HG007492 to the Center for Inherited Disease Research (CIDR) under contract number HHSN268201200008I). Additional analytical support was provided by NIH NCI U01 CA188392 (F.R.S.). Funding for the iCOGS infrastructure came from the European Community ' s Seventh Framework Pro- gramme under grant agreement n° 223175 (HEALTH-F2-2009-223175) (COGS), Cancer Research UK (C1287/A10118, C1287/A 10710, C12292/A11174, C1281/A12014, C5047/ A8384, C5047/A15007, C5047/A10692, and C8197/A16565), the National Institutes of Health (CA128978) and Post-Cancer GWAS initiative (1U19 CA148537, 1U19 CA148065, and 1U19 CA148112; the GAME-ON initiative), the Department of Defense (W81XWH-10-1-0341), the Canadian Institutes of Health Research (CIHR) for the CIHR Team in Familial Risks of Breast Cancer, Komen Foundation for the Cure, the Breast Cancer Research Foundation, and the Ovarian Cancer Research Fund. This work was supported by the Canadian Institutes of Health Research, European Commission ' s Seventh Framework Programme grant agreement n° 223175 (HEALTH-F2-2009-223175), Cancer Research UK Grants C5047/A7357, C1287/A10118, C1287/A16563, C5047/ A3354, C5047/A10692, C16913/A6135, C5047/A21332 and The National Institute of Health (NIH) Cancer Post-Cancer GWAS initiative grant: No. 1 U19 CA148537-01 (the GAME-ON initiative). We also thank the following for funding support: The Institute of Cancer Research and The Everyman Campaign, The Prostate Cancer Research Founda- tion, Prostate Research Campaign UK (now Prostate Action), The Orchid Cancer Appeal, The National Cancer Research Network UK, and The National Cancer Research Institute (NCRI) UK. We are grateful for support of NIHR funding to the NIHR Biomedical Research Centre at The Institute of Cancer Research and The Royal Marsden NHS Foundation Trust. The Prostate Cancer Program of Cancer Council Victoria also acknowledge grant support from The National Health and Medical Research Council, Australia (126402, 209057, 251533, 396414, 450104, 504700, 504702, 504715, 623204, 940394, and 614296), VicHealth, Cancer Council Victoria, The Prostate Cancer Foun- dation of Australia, The Whitten Foundation, PricewaterhouseCoopers, and Tattersall ' s. E.A.O., D.M.K., and E.M.K. acknowledge the Intramural Program of the National Human Genome Research Institute for their support. The BPC3 was supported by the U.S. National Institutes of Health, National Cancer Institute (cooperative agreements U01- CA98233 to D.J.H., U01-CA98710 to S.M.G., U01-CA98216 to E.R., and U01-CA98758 to B.E.H., and Intramural Research Program of NIH/National Cancer Institute, Division of Cancer Epidemiology and Genetics). CAPS GWAS study was supported by the Swedish Cancer Foundation (grant no 09-0677, 11-484, 12-823), the Cancer Risk Prediction Center (CRisP; www.crispcenter.org ), a Linneus Centre (Contract ID 70867902) fi nanced by the Swedish Research Council, Swedish Research Council (grant no K2010-70 × - 20430-04-3, 2014-2269). The Hannover Prostate Cancer Study was supported by the Lower Saxonian Cancer Society. PEGASUS was supported by the Intramural Research Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health. RAPPER was supported by the NIHR Manchester Bio- medical Research Center, Cancer Research UK (C147/A25254, C1094/A18504) and the EUs7Framework Programme Grant/Agreement no 60186. Overall: this research has been conducted using the UK Biobank Resource (application number 16549). NHS is supported by UM1 CA186107 (NHS cohort infrastructure grant), P01 CA87969, and R01 CA49449. NHSII is supported by UM1 CA176726 (NHSII cohort infrastructure grant),and R01-CA67262. A.L.K. is supported by R01 MH107649. We would like to thank the participants and staff of the NHS and NHSII for their valuable contributions as well as the following state cancer registries for their help: AL, AZ, AR, CA, CO, CT, DE, FL, GA, ID, IL, IN, IA, KY, LA, ME, MD, MA, MI, NE, NH, NJ, NY, NC, ND, OH, OK, OR, PA, RI, SC, TN, TX, VA, WA, WY. The authors assume full responsibility for analyses and interpretation of these data. ; Sí
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Publisher's version (útgefin grein). ; Quantifying the genetic correlation between cancers can provide important insights into the mechanisms driving cancer etiology. Using genome-wide association study summary statistics across six cancer types based on a total of 296,215 cases and 301,319 controls of European ancestry, here we estimate the pair-wise genetic correlations between breast, colorectal, head/neck, lung, ovary and prostate cancer, and between cancers and 38 other diseases. We observed statistically significant genetic correlations between lung and head/neck cancer (rg = 0.57, p = 4.6 × 10−8), breast and ovarian cancer (rg = 0.24, p = 7 × 10−5), breast and lung cancer (rg = 0.18, p =1.5 × 10−6) and breast and colorectal cancer (rg = 0.15, p = 1.1 × 10−4). We also found that multiple cancers are genetically correlated with non-cancer traits including smoking, psychiatric diseases and metabolic characteristics. Functional enrichment analysis revealed a significant excess contribution of conserved and regulatory regions to cancer heritability. Our comprehensive analysis of cross-cancer heritability suggests that solid tumors arising across tissues share in part a common germline genetic basis. ; The authors in this manuscript were working on behalf of BCAC, CCFR, CIMBA, CORECT, GECCO, OCAC, PRACTICAL, CRUK, BPC3, CAPS, PEGASUS, TRICL-ILCCO, ABCTB, APCB, BCFR, CONSIT TEAM, EMBRACE, GC-HBOC, GEMO, HEBON, kConFab/AOCS Mod SQuaD, and SWE-BRCA. The breast cancer genome-wide association analyses: BCAC is funded by Cancer Research UK [C1287/A16563, C1287/A10118], the European Union's Horizon 2020 Research and Innovation Programme (grant numbers 634935 and 633784 for BRIDGES and B-CAST, respectively), and by the European Community's Seventh Framework Programme under grant agreement number 223175 (grant number HEALTH-F2-2009-223175) (COGS). The EU Horizon 2020 Research and Innovation Programme funding source had no role in study design, data collection, data analysis, data interpretation, or writing of the report. Genotyping of the OncoArray was funded by the NIH Grant U19 CA148065, and Cancer UK Grant C1287/A16563 and the PERSPECTIVE project supported by the Government of Canada through Genome Canada and the Canadian Institutes of Health Research (grant GPH-129344) and, the Ministère de l'Économie, Science et Innovation du Québec through Genome Québec and the PSR-SIIRI-701 grant, and the Quebec Breast Cancer Foundation. Funding for the iCOGS infrastructure came from: the European Community's Seventh Framework Programme under grant agreement n° 223175 (HEALTH-F2-2009-223175) (COGS), Cancer Research UK (C1287/A10118, C1287/A10710, C12292/A11174, C1281/A12014, C5047/A8384, C5047/A15007, C5047/A10692, C8197/A16565), the National Institutes of Health (CA128978), and Post-Cancer GWAS initiative (1U19 CA148537, 1U19 CA148065, and 1U19 CA148112—the GAME-ON initiative), the Department of Defence (W81XWH-10-1-0341), the Canadian Institutes of Health Research (CIHR) for the CIHR Team in Familial Risks of Breast Cancer, and Komen Foundation for the Cure, the Breast Cancer Research Foundation, and the Ovarian Cancer Research Fund. The DRIVE Consortium was funded by U19 CA148065. The Australian Breast Cancer Family Study (ABCFS) was supported by grant UM1 CA164920 from the National Cancer Institute (USA). The content of this manuscript does not necessarily reflect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the USA Government or the BCFR. The ABCFS was also supported by the National Health and Medical Research Council of Australia, the New South Wales Cancer Council, the Victorian Health Promotion Foundation (Australia), and the Victorian Breast Cancer Research Consortium. J.L.H. is a National Health and Medical Research Council (NHMRC) Senior Principal Research Fellow. M.C.S. is a NHMRC Senior Research Fellow. The ABCS study was supported by the Dutch Cancer Society [grants NKI 2007-3839; 2009 4363]. The Australian Breast Cancer Tissue Bank (ABCTB) is generously supported by the National Health and Medical Research Council of Australia, The Cancer Institute NSW and the National Breast Cancer Foundation. The ACP study is funded by the Breast Cancer Research Trust, UK. The AHS study is supported by the intramural research program of the National Institutes of Health, the National Cancer Institute (grant number Z01-CP010119), and the National Institute of Environmental Health Sciences (grant number Z01-ES049030). The work of the BBCC was partly funded by ELAN-Fond of the University Hospital of Erlangen. The BBCS is funded by Cancer Research UK and Breast Cancer Now and acknowledges NHS funding to the NIHR Biomedical Research Centre, and the National Cancer Research Network (NCRN). The BCEES was funded by the National Health and Medical Research Council, Australia and the Cancer Council Western Australia and acknowledges funding from the National Breast Cancer Foundation (JS). For the BCFR-NY, BCFR-PA, and BCFR-UT this work was supported by grant UM1 CA164920 from the National Cancer Institute. The content of this manuscript does not necessarily reflect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the US Government or the BCFR. For BIGGS, ES is supported by NIHR Comprehensive Biomedical Research Centre, Guy's & St. Thomas' NHS Foundation Trust in partnership with King's College London, United Kingdom. IT is supported by the Oxford Biomedical Research Centre. BOCS is supported by funds from Cancer Research UK (C8620/A8372/A15106) and the Institute of Cancer Research (UK). BOCS acknowledges NHS funding to the Royal Marsden/Institute of Cancer Research NIHR Specialist Cancer Biomedical Research Centre. The BREast Oncology GAlician Network (BREOGAN) is funded by Acción Estratégica de Salud del Instituto de Salud Carlos III FIS PI12/02125/Cofinanciado FEDER; Acción Estratégica de Salud del Instituto de Salud Carlos III FIS Intrasalud (PI13/01136); Programa Grupos Emergentes, Cancer Genetics Unit, Instituto de Investigacion Biomedica Galicia Sur. Xerencia de Xestion Integrada de Vigo-SERGAS, Instituto de Salud Carlos III, Spain; Grant 10CSA012E, Consellería de Industria Programa Sectorial de Investigación Aplicada, PEME I + D e I + D Suma del Plan Gallego de Investigación, Desarrollo e Innovación Tecnológica de la Consellería de Industria de la Xunta de Galicia, Spain; Grant EC11-192. Fomento de la Investigación Clínica Independiente, Ministerio de Sanidad, Servicios Sociales e Igualdad, Spain; and Grant FEDER-Innterconecta. Ministerio de Economia y Competitividad, Xunta de Galicia, Spain. The BSUCH study was supported by the Dietmar-Hopp Foundation, the Helmholtz Society and the German Cancer Research Center (DKFZ). The CAMA study was funded by Consejo Nacional de Ciencia y Tecnología (CONACyT) (SALUD-2002-C01-7462). Sample collection and processing was funded in part by grants from the National Cancer Institute (NCI R01CA120120 and K24CA169004). CBCS is funded by the Canadian Cancer Society (grant # 313404) and the Canadian Institutes of Health Research. CCGP is supported by funding from the University of Crete. The CECILE study was supported by Fondation de France, Institut National du Cancer (INCa), Ligue Nationale contre le Cancer, Agence Nationale de Sécurité Sanitaire, de l'Alimentation, de l'Environnement et du Travail (ANSES), Agence Nationale de la Recherche (ANR). The CGPS was supported by the Chief Physician Johan Boserup and Lise Boserup Fund, the Danish Medical Research Council, and Herlev and Gentofte Hospital. The CNIO-BCS was supported by the Instituto de Salud Carlos III, the Red Temática de Investigación Cooperativa en Cáncer and grants from the Asociación Española Contra el Cáncer and the Fondo de Investigación Sanitario (PI11/00923 and PI12/00070). COLBCCC is supported by the German Cancer Research Center (DKFZ), Heidelberg, Germany. D.T. was in part supported by a postdoctoral fellowship from the Alexander von Humboldt Foundation. The American Cancer Society funds the creation, maintenance, and updating of the CPS-II cohort. The CTS was initially supported by the California Breast Cancer Act of 1993 and the California Breast Cancer Research Fund (contract 97-10500) and is currently funded through the National Institutes of Health (R01 CA77398, UM1 CA164917, and U01 CA199277). Collection of cancer incidence data was supported by the California Department of Public Health as part of the statewide cancer reporting program mandated by California Health and Safety Code Section 103885. H.A.C eceives support from the Lon V Smith Foundation (LVS39420). The University of Westminster curates the DietCompLyf database funded by Against Breast Cancer Registered Charity No. 1121258 and the NCRN. The coordination of EPIC is financially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The national cohorts are supported by: Ligue Contre le Cancer, Institut Gustave Roussy, Mutuelle Générale de l'Education Nationale, Institut National de la Santé et de la Recherche Médicale (INSERM) (France); German Cancer Aid, German Cancer Research Center (DKFZ), Federal Ministry of Education and Research (BMBF) (Germany); the Hellenic Health Foundation, the Stavros Niarchos Foundation (Greece); Associazione Italiana per la Ricerca sul Cancro-AIRC-Italy and National Research Council (Italy); Dutch Ministry of Public Health, Welfare and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds, Dutch Prevention Funds, Dutch ZON (Zorg Onderzoek Nederland), World Cancer Research Fund (WCRF), Statistics Netherlands (The Netherlands); Health Research Fund (FIS), PI13/00061 to Granada, PI13/01162 to EPIC-Murcia, Regional Governments of Andalucía, Asturias, Basque Country, Murcia and Navarra, ISCIII RETIC (RD06/0020) (Spain); Cancer Research UK (14136 to EPIC-Norfolk; C570/A16491 and C8221/A19170 to EPIC-Oxford), Medical Research Council (1000143 to EPIC-Norfolk, MR/M012190/1 to EPIC-Oxford) (United Kingdom). The ESTHER study was supported by a grant from the Baden Württemberg Ministry of Science, Research and Arts. Additional cases were recruited in the context of the VERDI study, which was supported by a grant from the German Cancer Aid (Deutsche Krebshilfe). FHRISK is funded from NIHR grant PGfAR 0707-10031. The GC-HBOC (German Consortium of Hereditary Breast and Ovarian Cancer) is supported by the German Cancer Aid (grant no 110837, coordinator: Rita K. Schmutzler, Cologne). This work was also funded by the European Regional Development Fund and Free State of Saxony, Germany (LIFE - Leipzig Research Centre for Civilization Diseases, project numbers 713-241202, 713-241202, 14505/2470, and 14575/2470). The GENICA was funded by the Federal Ministry of Education and Research (BMBF) Germany grants 01KW9975/5, 01KW9976/8, 01KW9977/0, and 01KW0114, the Robert Bosch Foundation, Stuttgart, Deutsches Krebsforschungszentrum (DKFZ), Heidelberg, the Institute for Prevention and Occupational Medicine of the German Social Accident Insurance, Institute of the Ruhr University Bochum (IPA), Bochum, as well as the Department of Internal Medicine, Evangelische Kliniken Bonn gGmbH, Johanniter Krankenhaus, Bonn, Germany. The GEPARSIXTO study was conducted by the German Breast Group GmbH. The GESBC was supported by the Deutsche Krebshilfe e. V. [70492] and the German Cancer Research Center (DKFZ). GLACIER was supported by Breast Cancer Now, CRUK and Biomedical Research Centre at Guy's and St Thomas' NHS Foundation Trust and King's College London. The HABCS study was supported by the Claudia von Schilling Foundation for Breast Cancer Research, by the Lower Saxonian Cancer Society, and by the Rudolf-Bartling Foundation. The HEBCS was financially supported by the Helsinki University Central Hospital Research Fund, Academy of Finland (266528), the Finnish Cancer Society, and the Sigrid Juselius Foundation. The HERPACC was supported by MEXT Kakenhi (No. 170150181 and 26253041) from the Ministry of Education, Science, Sports, Culture and Technology of Japan, by a Grant-in-Aid for the Third Term Comprehensive 10-Year Strategy for Cancer Control from Ministry Health, Labour and Welfare of Japan, by Health and Labour Sciences Research Grants for Research on Applying Health Technology from Ministry Health, Labour and Welfare of Japan, by National Cancer Center Research and Development Fund, and "Practical Research for Innovative Cancer Control (15ck0106177h0001)" from Japan Agency for Medical Research and development, AMED, and Cancer Bio Bank Aichi. The HMBCS was supported by a grant from the Friends of Hannover Medical School and by the Rudolf Bartling Foundation. The HUBCS was supported by a grant from the German Federal Ministry of Research and Education (RUS08/017), and by the Russian Foundation for Basic Research and the Federal Agency for Scientific Organizations for support the Bioresource collections and RFBR grants 14-04-97088, 17-29-06014, and 17-44-020498. ICICLE was supported by Breast Cancer Now, CRUK, and Biomedical Research Centre at Guy's and St Thomas' NHS Foundation Trust and King's College London. Financial support for KARBAC was provided through the regional agreement on medical training and clinical research (A.L.F.) between Stockholm County Council and Karolinska Institutet, the Swedish Cancer Society, The Gustav V Jubilee foundation and Bert von Kantzows foundation. The KARMA study was supported by Märit and Hans Rausings Initiative Against Breast Cancer. The KBCP was financially supported by the special Government Funding (E.V.O.) of Kuopio University Hospital grants, Cancer Fund of North Savo, the Finnish Cancer Organizations, and by the strategic funding of the University of Eastern Finland. kConFab is supported by a grant from the National Breast Cancer Foundation, and previously by the National Health and Medical Research Council (NHMRC), the Queensland Cancer Fund, the Cancer Councils of New South Wales, Victoria, Tasmania and South Australia, and the Cancer Foundation of Western Australia. Financial support for the AOCS was provided by the United States Army Medical Research and Materiel Command [DAMD17-01-1-0729], Cancer Council Victoria, Queensland Cancer Fund, Cancer Council New South Wales, Cancer Council South Australia, The Cancer Foundation of Western Australia, Cancer Council Tasmania and the National Health and Medical Research Council of Australia (NHMRC; 400413, 400281, 199600). G.C.-T. and P.W. are supported by the NHMRC. RB was a Cancer Institute NSW Clinical Research Fellow. The KOHBRA study was partially supported by a grant from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), and the National R&D Program for Cancer Control, Ministry of Health & Welfare, Republic of Korea (HI16C1127; 1020350; 1420190). LAABC is supported by grants (1RB-0287, 3PB-0102, 5PB-0018, 10PB-0098) from the California Breast Cancer Research Program. Incident breast cancer cases were collected by the USC Cancer Surveillance Program (CSP) which is supported under subcontract by the California Department of Health. The CSP is also part of the National Cancer Institute's Division of Cancer Prevention and Control Surveillance, Epidemiology, and End Results Program, under contract number N01CN25403. L.M.B.C. is supported by the 'Stichting tegen Kanker'. D.L. is supported by the FWO. The MABCS study is funded by the Research Centre for Genetic Engineering and Biotechnology "Georgi D. Efremov" and supported by the German Academic Exchange Program, DAAD. The MARIE study was supported by the Deutsche Krebshilfe e.V. [70-2892-BR I, 106332, 108253, 108419, 110826, 110828], the Hamburg Cancer Society, the German Cancer Research Center (DKFZ) and the Federal Ministry of Education and Research (BMBF) Germany [01KH0402]. MBCSG is supported by grants from the Italian Association for Cancer Research (AIRC) and by funds from the Italian citizens who allocated the 5/1000 share of their tax payment in support of the Fondazione IRCCS Istituto Nazionale Tumori, according to Italian laws (INT-Institutional strategic projects "5 × 1000"). The MCBCS was supported by the NIH grants CA192393, CA116167, CA176785 an NIH Specialized Program of Research Excellence (SPORE) in Breast Cancer [CA116201], and the Breast Cancer Research Foundation and a generous gift from the David F. and Margaret T. Grohne Family Foundation. MCCS cohort recruitment was funded by VicHealth and Cancer Council Victoria. The MCCS was further supported by Australian NHMRC grants 209057 and 396414, and by infrastructure provided by Cancer Council Victoria. Cases and their vital status were ascertained through the Victorian Cancer Registry (VCR) and the Australian Institute of Health and Welfare (AIHW), including the National Death Index and the Australian Cancer Database. The MEC was support by NIH grants CA63464, CA54281, CA098758, CA132839, and CA164973. The MISS study is supported by funding from ERC-2011-294576 Advanced grant, Swedish Cancer Society, Swedish Research Council, Local hospital funds, Berta Kamprad Foundation, Gunnar Nilsson. The MMHS study was supported by NIH grants CA97396, CA128931, CA116201, CA140286, and CA177150. MSKCC is supported by grants from the Breast Cancer Research Foundation and Robert and Kate Niehaus Clinical Cancer Genetics Initiative. The work of MTLGEBCS was supported by the Quebec Breast Cancer Foundation, the Canadian Institutes of Health Research for the "CIHR Team in Familial Risks of Breast Cancer" program – grant # CRN-87521 and the Ministry of Economic Development, Innovation and Export Trade – grant # PSR-SIIRI-701. MYBRCA is funded by research grants from the Malaysian Ministry of Higher Education (UM.C/HlR/MOHE/06) and Cancer Research Malaysia. MYMAMMO is supported by research grants from Yayasan Sime Darby LPGA Tournament and Malaysian Ministry of Higher Education (RP046B-15HTM). The NBCS has been supported by the Research Council of Norway grant 193387/V50 (to A.-L. Børresen-Dale and V.N. Kristensen) and grant 193387/H10 (to A.-L. Børresen-Dale and V.N. Kristensen), South Eastern Norway Health Authority (grant 39346 to A.-L. Børresen-Dale and 27208 to V.N. Kristensen) and the Norwegian Cancer Society (to A.-L. Børresen-Dale and 419616 - 71248 - PR-2006-0282 to V.N. Kristensen). It has received funding from the K.G. Jebsen Centre for Breast Cancer Research (2012-2015). The NBHS was supported by NIH grant R01CA100374. Biological sample preparation was conducted the Survey and Biospecimen Shared Resource, which is supported by P30 CA68485. The Northern California Breast Cancer Family Registry (NC-BCFR) and Ontario Familial Breast Cancer Registry (OFBCR) were supported by grant UM1 CA164920 from the National Cancer Institute (USA). The content of this manuscript does not necessarily reflect the views or policies of the National Cancer Institute or any of the collaborating centers in the Breast Cancer Family Registry (BCFR), nor does mention of trade names, commercial products, or organizations imply endorsement by the USA Government or the BCFR. The Carolina Breast Cancer Study was funded by Komen Foundation, the National Cancer Institute (P50 CA058223, U54 CA156733, and U01 CA179715), and the North Carolina University Cancer Research Fund. The NGOBCS was supported by Grants-in-Aid for the Third Term Comprehensive Ten-Year Strategy for Cancer Control from the Ministry of Health, Labor and Welfare of Japan, and for Scientific Research on Priority Areas, 17015049 and for Scientific Research on Innovative Areas, 221S0001, from the Ministry of Education, Culture, Sports, Science, and Technology of Japan. The NHS was supported by NIH grants P01 CA87969, UM1 CA186107, and U19 CA148065. The NHS2 was supported by NIH grants UM1 CA176726 and U19 CA148065. The OBCS was supported by research grants from the Finnish Cancer Foundation, the Academy of Finland (grant number 250083, 122715 and Center of Excellence grant number 251314), the Finnish Cancer Foundation, the Sigrid Juselius Foundation, the University of Oulu, the University of Oulu Support Foundation, and the special Governmental EVO funds for Oulu University Hospital-based research activities. The ORIGO study was supported by the Dutch Cancer Society (RUL 1997-1505) and the Biobanking and Biomolecular Resources Research Infrastructure (BBMRI-NL CP16). The PBCS was funded by Intramural Research Funds of the National Cancer Institute, Department of Health and Human Services, USA. Genotyping for PLCO was supported by the Intramural Research Program of the National Institutes of Health, NCI, Division of Cancer Epidemiology and Genetics. The PLCO is supported by the Intramural Research Program of the Division of Cancer Epidemiology and Genetics and supported by contracts from the Division of Cancer Prevention, National Cancer Institute, National Institutes of Health. The POSH study is funded by Cancer Research UK (grants C1275/A11699, C1275/C22524, C1275/A19187, C1275/A15956, and Breast Cancer Campaign 2010PR62, 2013PR044. PROCAS is funded from NIHR grant PGfAR 0707-10031. The RBCS was funded by the Dutch Cancer Society (DDHK 2004-3124, DDHK 2009-4318). The SASBAC study was supported by funding from the Agency for Science, Technology and Research of Singapore (A*STAR), the US National Institute of Health (NIH) and the Susan G. Komen Breast Cancer Foundation. The SBCGS was supported primarily by NIH grants R01CA64277, R01CA148667, UMCA182910, and R37CA70867. Biological sample preparation was conducted the Survey and Biospecimen Shared Resource, which is supported by P30 CA68485. The scientific development and funding of this project were, in part, supported by the Genetic Associations and Mechanisms in Oncology (GAME-ON) Network U19 CA148065. The SBCS was supported by Sheffield Experimental Cancer Medicine Centre and Breast Cancer Now Tissue Bank. The SCCS is supported by a grant from the National Institutes of Health (R01 CA092447). Data on SCCS cancer cases used in this publication were provided by the Alabama Statewide Cancer Registry; Kentucky Cancer Registry, Lexington, KY; Tennessee Department of Health, Office of Cancer Surveillance; Florida Cancer Data System; North Carolina Central Cancer Registry, North Carolina Division of Public Health; Georgia Comprehensive Cancer Registry; Louisiana Tumor Registry; Mississippi Cancer Registry; South Carolina Central Cancer Registry; Virginia Department of Health, Virginia Cancer Registry; Arkansas Department of Health, Cancer Registry, 4815 W. Markham, Little Rock, AR 72205. The Arkansas Central Cancer Registry is fully funded by a grant from National Program of Cancer Registries, Centers for Disease Control and Prevention (CDC). Data on SCCS cancer cases from Mississippi were collected by the Mississippi Cancer Registry which participates in the National Program of Cancer Registries (NPCR) of the Centers for Disease Control and Prevention (CDC). The contents of this publication are solely the responsibility of the authors and do not necessarily represent the official views of the CDC or the Mississippi Cancer Registry. SEARCH is funded by Cancer Research UK [C490/A10124, C490/A16561] and supported by the UK National Institute for Health Research Biomedical Research Centre at the University of Cambridge. The University of Cambridge has received salary support for PDPP from the NHS in the East of England through the Clinical Academic Reserve. SEBCS was supported by the BRL (Basic Research Laboratory) program through the National Research Foundation of Korea funded by the Ministry of Education, Science and Technology (2012-0000347). SGBCC is funded by the NUS start-up Grant, National University Cancer Institute Singapore (NCIS) Centre Grant and the NMRC Clinician Scientist Award. Additional controls were recruited by the Singapore Consortium of Cohort Studies-Multi-ethnic cohort (SCCS-MEC), which was funded by the Biomedical Research Council, grant number: 05/1/21/19/425. The Sister Study (SISTER) is supported by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences (Z01-ES044005 and Z01-ES049033). The Two Sister Study (2SISTER) was supported by the Intramural Research Program of the NIH, National Institute of Environmental Health Sciences (Z01-ES044005 and Z01-ES102245), and, also by a grant from Susan G. Komen for the Cure, grant FAS0703856. SKKDKFZS is supported by the DKFZ. The SMC is funded by the Swedish Cancer Foundation. The SZBCS was supported by Grant PBZ_KBN_122/P05/2004. The TBCS was funded by The National Cancer Institute, Thailand. The TNBCC was supported by a Specialized Program of Research Excellence (SPORE) in Breast Cancer (CA116201), a grant from the Breast Cancer Research Foundation, a generous gift from the David F. and Margaret T. Grohne Family Foundation. The TWBCS is supported by the Taiwan Biobank project of the Institute of Biomedical Sciences, Academia Sinica, Taiwan. The UCIBCS component of this research was supported by the NIH [CA58860, CA92044] and the Lon V Smith Foundation [LVS39420]. The UKBGS is funded by Breast Cancer Now and the Institute of Cancer Research (ICR), London. ICR acknowledges NHS funding to the NIHR Biomedical Research Centre. The UKOPS study was funded by The Eve Appeal (The Oak Foundation) and supported by the National Institute for Health Research University College London Hospitals Biomedical Research Centre. The US3SS study was supported by Massachusetts (K.M.E., R01CA47305), Wisconsin (P.A.N., R01 CA47147) and New Hampshire (L.T.-E., R01CA69664) centers, and Intramural Research Funds of the National Cancer Institute, Department of Health and Human Services, USA. The USRT Study was funded by Intramural Research Funds of the National Cancer Institute, Department of Health and Human Services, USA. The WAABCS study was supported by grants from the National Cancer Institute of the National Institutes of Health (R01 CA89085 and P50 CA125183 and the D43 TW009112 grant), Susan G. Komen (SAC110026), the Dr. Ralph and Marian Falk Medical Research Trust, and the Avon Foundation for Women. The WHI program is funded by the National Heart, Lung, and Blood Institute, the US National Institutes of Health and the US Department of Health and Human Services (HHSN268201100046C, HHSN268201100001C, HHSN268201100002C, HHSN268201100003C, HHSN268201100004C, and HHSN271201100004C). This work was also funded by NCI U19 CA148065-01. D.G.E. is supported by the all Manchester NIHR Biomedical research center Manchester (IS-BRC-1215-20007). HUNBOCS, Hungarian Breast and Ovarian Cancer Study was supported by Hungarian Research Grant KTIA-OTKA CK-80745, NKFI_OTKA K-112228. C.I. received support from the Nontherapeutic Subject Registry Shared Resource at Georgetown University (NIH/NCI P30-CA-51008) and the Jess and Mildred Fisher Center for Hereditary Cancer and Clinical Genomics Research. K.M. is supported by CRUK C18281/A19169. City of Hope Clinical Cancer Community Research Network and the Hereditary Cancer Research Registry, supported in part by Award Number RC4CA153828 (PI: J Weitzel) from the National Cancer Institute and the office of the Directory, National Institutes of Health. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. The colorectal cancer genome-wide association analyses: Colorectal Transdisciplinary Study (CORECT): The content of this manuscript does not necessarily reflect the views or policies of the National Cancer Institute or any of the collaborating centers in the CORECT Consortium, nor does mention of trade names, commercial products or organizations imply endorsement by the US Government or the CORECT Consortium. We are incredibly grateful for the contributions of Dr. Brian Henderson and Dr. Roger Green over the course of this study and acknowledge them in memoriam. We are also grateful for support from Daniel and Maryann Fong. ColoCare: we thank the many investigators and staff who made this research possible in ColoCare Seattle and ColoCare Heidelberg. ColoCare was initiated and developed at the Fred Hutchinson Cancer Research Center by Drs. Ulrich and Grady. CCFR: the Colon CFR graciously thanks the generous contributions of their study participants, dedication of study staff, and financial support from the U.S. National Cancer Institute, without which this important registry would not exist. Galeon: GALEON wishes to thank the Department of Surgery of University Hospital of Santiago (CHUS), Sara Miranda Ponte, Carmen M Redondo, and the staff of the Department of Pathology and Biobank of CHUS, Instituto de Investigación Sanitaria de Santiago (IDIS), Instituto de Investigación Sanitaria Galicia Sur (IISGS), SERGAS, Vigo, Spain, and Programa Grupos Emergentes, Cancer Genetics Unit, CHUVI Vigo Hospital, Instituto de Salud Carlos III, Spain. MCCS: this study was made possible by the contribution of many people, including the original investigators and the diligent team who recruited participants and continue to work on follow-up. We would also like to express our gratitude to the many thousands of Melbourne residents who took part in the study and provided blood samples. SEARCH: We acknowledge the contributions of Mitul Shah, Val Rhenius, Sue Irvine, Craig Luccarini, Patricia Harrington, Don Conroy, Rebecca Mayes, and Caroline Baynes. The Swedish low-risk colorectal cancer study: we thank Berith Wejderot and the Swedish low-risk colorectal cancer study group. Genetics & Epidemiology of Colorectal Cancer Consortium (GECCO): we thank all those at the GECCO Coordinating Center for helping bring together the data and people that made this project possible. ASTERISK: we are very grateful to Dr. Bruno Buecher without whom this project would not have existed. We also thank all those who agreed to participate in this study, including the patients and the healthy control persons, as well as all the physicians, technicians and students. DACHS: we thank all participants and cooperating clinicians, and Ute Handte-Daub, Renate Hettler-Jensen, Utz Benscheid, Muhabbet Celik, and Ursula Eilber for excellent technical assistance. HPFS, NHS and PHS: we acknowledge Patrice Soule and Hardeep Ranu of the Dana-Farber Harvard Cancer Center High-Throughput Polymorphism Core who assisted in the genotyping for NHS, HPFS, and PHS under the supervision of Dr. Immaculata Devivo and Dr. David Hunter, Qin (Carolyn) Guo, and Lixue Zhu who assisted in programming for NHS and HPFS and Haiyan Zhang who assisted in programming for the PHS. We thank the participants and staff of the Nurses' Health Study and the Health Professionals Follow-Up Study, for their valuable contributions as well as the following state cancer registries for their help: A.L., A.Z., A.R., C.A., C.O., C.T., D.E., F.L., G.A., I.D., I.L., I.N., I.A., K.Y., L.A., M.E., M.D., M.A., M.I., N.E., N.H., N.J., N.Y., N.C., N.D., O.H., O.K., O.R., P.A., R.I., S.C., T.N., T.X., V.A., W.A., W.Y. In addition, this study was approved by the Connecticut Department of Public Health (DPH) Human Investigations Committee. Certain data used in this publication were obtained from the DPH. We assume full responsibility for analyses and interpretation of these data. PLCO: we thank Drs. Christine Berg and Philip Prorok, Division of Cancer Prevention, National Cancer Institute, the Screening Center investigators and staff or the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial, Mr. Tom Riley and staff, Information Management Services Inc., Ms. Barbara O'Brien and staff, Westat Inc. and Drs. Bill Kopp, Wen Shao and staff, SAIC-Frederick. Most importantly, we acknowledge the study participants for their contributions for making this study possible. The statements contained herein are solely those of the authors and do not represent or imply concurrence or endorsement by NCI. PMH: we thank the study participants and staff of the Hormones and Colon Cancer study. WHI: we thank the WHI investigators and staff for their dedication, and the study participants for making the program possible. A full listing of WHI investigators can be found at https://cleo.whi.org/researchers/Documents%20%20Write%20a%20Paper/WHI%20Investigator%20Short20List.pdf. CORECT: The CORECT Study was supported by the National Cancer Institute, National Institutes of Health (NCI/NIH), U.S. Department of Health and Human Services (grant numbers U19 CA148107, R01 CA81488, P30 CA014089, R01 CA197350; P01 CA196569; and R01 CA201407) and National Institutes of Environmental Health Sciences, National Institutes of Health (grant number T32 ES013678). The ATBC Study was supported by the US Public Health Service contracts (N01-CN-45165, N01-RC-45035, N01-RC-37004, and HHSN261201000006C) from the National Cancer Institute. The Cancer Prevention Study-II Nutrition Cohort is funded by the American Cancer Society. ColoCare: This work was supported by the National Institutes of Health (grant numbers R01 CA189184, U01 CA206110, 2P30CA015704-40 (Gilliland)), the Matthias Lackas-Foundation, the German Consortium for Translational Cancer Research, and the EU TRANSCAN initiative. Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO): funding for GECCO was provided by the National Cancer Institute, National Institutes of Health, U.S. Department of Health and Human Services (grant numbers U01 CA137088, R01 CA059045, and U01 CA164930). This research was funded in part through the NIH/NCI Cancer Center Support Grant P30 CA015704. The Colon Cancer Family Registry (CFR) Illumina GWAS was supported by funding from the National Cancer Institute, National Institutes of Health (grant numbers U01 CA122839, R01 CA143247). The Colon CFR/CORECT Affymetrix Axiom GWAS and OncoArray GWAS were supported by funding from National Cancer Institute, National Institutes of Health (grant number U19 CA148107 to S.G.). The Colon CFR participant recruitment and collection of data and biospecimens used in this study were supported by the National Cancer Institute, National Institutes of Health (grant number UM1 CA167551) and through cooperative agreements with the following Colon CFR centers: Australasian Colorectal Cancer Family Registry (NCI/NIH grant numbers U01 CA074778 and U01/U24 CA097735), USC Consortium Colorectal Cancer Family Registry (NCI/NIH grant numbers U01/U24 CA074799), Mayo Clinic Cooperative Family Registry for Colon Cancer Studies (NCI/NIH grant number U01/U24 CA074800), Ontario Familial Colorectal Cancer Registry (NCI/NIH grant number U01/U24 CA074783), Seattle Colorectal Cancer Family Registry (NCI/NIH grant number U01/U24 CA074794), and University of Hawaii Colorectal Cancer Family Registry (NCI/NIH grant number U01/U24 CA074806), Additional support for case ascertainment was provided from the Surveillance, Epidemiology and End Results (SEER) Program of the National Cancer Institute to Fred Hutchinson Cancer Research Center (Control Nos. N01-CN-67009 and N01-PC-35142, and Contract No. HHSN2612013000121), the Hawai'i Department of Health (Control Nos. N01-PC-67001 and N01-PC-35137, and Contract No. HHSN26120100037C, and the California Department of Public Health (contracts HHSN261201000035C awarded to the University of Southern California, and the following state cancer registries: A.Z., C.O., M.N., N.C., N.H., and by the Victoria Cancer Registry and Ontario Cancer Registry. ESTHER/VERDI was supported by grants from the Baden–Württemberg Ministry of Science, Research and Arts and the German Cancer Aid. MCCS cohort recruitment was funded by VicHealth and Cancer Council Victoria. GALEON: FIS Intrasalud (PI13/01136). The MCCS was further supported by Australian NHMRC grants 509348, 209057, 251553, and 504711 and by infrastructure provided by Cancer Council Victoria. Cases and their vital status were ascertained through the Victorian Cancer Registry (VCR) and the Australian Institute of Health and Welfare (AIHW), including the National Death Index and the Australian Cancer Database. MSKCC: the work at Sloan Kettering in New York was supported by the Robert and Kate Niehaus Center for Inherited Cancer Genomics and the Romeo Milio Foundation. Moffitt: This work was supported by funding from the National Institutes of Health (grant numbers R01 CA189184, P30 CA076292), Florida Department of Health Bankhead-Coley Grant 09BN-13, and the University of South Florida Oehler Foundation. Moffitt contributions were supported in part by the Total Cancer Care Initiative, Collaborative Data Services Core, and Tissue Core at the H. Lee Moffitt Cancer Center & Research Institute, a National Cancer Institute-designated Comprehensive Cancer Center (grant number P30 CA076292). SEARCH: Cancer Research UK (C490/A16561). The Spanish study was supported by Instituto de Salud Carlos III, co-funded by FEDER funds –a way to build Europe– (grants PI14-613 and PI09-1286), Catalan Government DURSI (grant 2014SGR647), and Junta de Castilla y León (grant LE22A10-2). The Swedish Low-risk Colorectal Cancer Study: the study was supported by grants from the Swedish research council; K2015-55 × -22674-01-4, K2008-55 × -20157-03-3, K2006-72 × -20157-01-2 and the Stockholm County Council (ALF project). CIDR genotyping for the Oncoarray was conducted under contract 268201200008I (to K.D.), through grant 101HG007491-01 (to C.I.A.). The Norris Cotton Cancer Center - P30CA023108, The Quantitative Biology Research Institute - P20GM103534, and the Coordinating Center for Screen Detected Lesions - U01CA196386 also supported efforts of C.I.A. This work was also supported by the National Cancer Institute (grant numbers U01 CA1817700, R01 CA144040). ASTERISK: a Hospital Clinical Research Program (PHRC) and supported by the Regional Council of Pays de la Loire, the Groupement des Entreprises Françaises dans la Lutte contre le Cancer (GEFLUC), the Association Anne de Bretagne Génétique and the Ligue Régionale Contre le Cancer (LRCC). COLO2&3: National Institutes of Health (grant number R01 CA060987). DACHS: This work was supported by the German Research Council (BR 1704/6-1, BR 1704/6-3, BR 1704/6-4, CH 117/1-1, HO 5117/2-1, HE 5998/2-1, KL 2354/3-1, RO 2270/8-1, and BR 1704/17-1), the Interdisciplinary Research Program of the National Center for Tumor Diseases (NCT), Germany, and the German Federal Ministry of Education and Research (01KH0404, 01ER0814, 01ER0815, 01ER1505A, and 01ER1505B). DALS: National Institutes of Health (grant number R01 CA048998 to M.L.S). HPFS is supported by National Institutes of Health (grant numbers P01 CA055075, UM1 CA167552, R01 137178, and P50 CA127003), NHS by the National Institutes of Health (grant numbers UM1 CA186107, R01 CA137178, P01 CA087969, and P50 CA127003), NHSII by the National Institutes of Health (grant numbers R01 050385CA and UM1 CA176726), and PHS by the National Institutes of Health (grant number R01 CA042182). MEC: National Institutes of Health (grant numbers R37 CA054281, P01 CA033619, and R01 CA063464). OFCCR: National Institutes of Health, through funding allocated to the Ontario Registry for Studies of Familial Colorectal Cancer (grant number U01 CA074783); see Colon CFR section above. As subset of ARCTIC, OFCCR is supported by a GL2 grant from the Ontario Research Fund, the Canadian Institutes of Health Research, and the Cancer Risk Evaluation (CaRE) Program grant from the Canadian Cancer Society Research Institute. T.J.H. and B.W.Z. are recipients of Senior Investigator Awards from the Ontario Institute for Cancer Research, through generous support from the Ontario Ministry of Research and Innovation. PLCO: Intramural Research Program of the Division of Cancer Epidemiology and Genetics and supported by contracts from the Division of Cancer Prevention, National Cancer Institute, NIH, DHHS. Additionally, a subset of control samples was genotyped as part of the Cancer Genetic Markers of Susceptibility (CGEMS) Prostate Cancer GWAS, Colon CGEMS pancreatic cancer scan (PanScan), and the Lung Cancer and Smoking study. The prostate and PanScan study datasets were accessed with appropriate approval through the dbGaP online resource (http://cgems.cancer.gov/data/) accession numbers phs000207.v1.p1 and phs000206.v3.p2, respectively, and the lung datasets were accessed from the dbGaP website (http://www.ncbi.nlm.nih.gov/gap) through accession number phs000093.v2.p2. Funding for the Lung Cancer and Smoking study was provided by National Institutes of Health (NIH), Genes, Environment and Health Initiative (GEI) Z01 CP 010200, NIH U01 HG004446, and NIH GEI U01 HG 004438. For the lung study, the GENEVA Coordinating Center provided assistance with genotype cleaning and general study coordination, 23 and the Johns Hopkins University Center for Inherited Disease Research conducted genotyping. PMH: National Institutes of Health (grant number R01 CA076366). VITAL: National Institutes of Health (grant number K05-CA154337). WHI: The WHI program is funded by the National Heart, Lung, and Blood Institute, National Institutes of Health, U.S. Department of Health and Human Services through contracts HHSN268201600018C, HHSN268201600001C, HHSN268201600002C, HHSN268201600003C, and HHSN268201600004C. The head and neck cancer genome-wide association analyses: The study was supported by NIH/NCI: P50 CA097190, and P30 CA047904, Canadian Cancer Society Research Institute (no. 020214) and Cancer Care Ontario Research Chair to R.H. The Princess Margaret Hospital Head and Neck Cancer Translational Research Program is funded by the Wharton family, Joe's Team, Gordon Tozer, Bruce Galloway and the Elia family. Geoffrey Liu was supported by the Posluns Family Fund and the Lusi Wong Family Fund at the Princess Margaret Foundation, and the Alan B. Brown Chair in Molecular Genomics. This publication presents data from Head and Neck 5000 (H&N5000). H&N5000 was a component of independent research funded by the UK National Institute for Health Research (NIHR) under its Programme Grants for Applied Research scheme (RP-PG-0707-10034). The views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health. Human papillomavirus (HPV) in H&N5000 serology was supported by a Cancer Research UK Programme Grant, the Integrative Cancer Epidemiology Programme (grant number: C18281/A19169). National Cancer Institute (R01-CA90731); National Institute of Environmental Health Sciences (P30ES10126). The authors thank all the members of the GENCAPO team/The Head and Neck Genome Project (GENCAPO) was supported by the Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) (Grant numbers 04/12054-9 and 10/51168-0). CPS-II recruitment and maintenance is supported with intramural research funding from the American Cancer Society. Genotyping performed at the Center for Inherited Disease Research (CIDR) was funded through the U.S. National Institute of Dental and Craniofacial Research (NIDCR) grant 1 × 01HG007780-0. The University of Pittsburgh head and neck cancer case-control study is supported by National Institutes of Health grants P50 CA097190 and P30 CA047904. The Carolina Head and Neck Cancer Study (CHANCE) was supported by the National Cancer Institute (R01-CA90731). The Head and Neck Genome Project (GENCAPO) was supported by the Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) (Grant numbers 04/12054-9 and 10/51168-0). The authors thank all the members of the GENCAPO team. The HN5000 study was funded by the National Institute for Health Research (NIHR) under its Programme Grants for Applied Research scheme (RP-PG-0707-10034), the views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health. The Toronto study was funded by the Canadian Cancer Society Research Institute (020214) and the National Cancer Institute (U19-CA148127) and the Cancer Care Ontario Research Chair. The alcohol-related cancers and genetic susceptibility study in Europe (ARCAGE) was funded by the European Commission's 5th Framework Program (QLK1-2001-00182), the Italian Association for Cancer Research, Compagnia di San Paolo/FIRMS, Region Piemonte, and Padova University (CPDA057222). The Rome Study was supported by the Associazione Italiana per la Ricerca sul Cancro (AIRC) IG 2011 10491 and IG2013 14220 to S.B., and Fondazione Veronesi to S.B. The IARC Latin American study was funded by the European Commission INCO-DC programme (IC18-CT97-0222), with additional funding from Fondo para la Investigacion Cientifica y Tecnologica (Argentina) and the Fundação de Amparo à Pesquisa do Estado de São Paulo (01/01768-2). We thank Leticia Fernandez, Instituto Nacional de Oncologia y Radiobiologia, La Habana, Cuba and Sergio and Rosalina Koifman, for their efforts with the IARC Latin America study São Paulo center. The IARC Central Europe study was supported by European Commission's INCO-COPERNICUS Program (IC15- CT98-0332), NIH/National Cancer Institute grant CA92039, and the World Cancer Research Foundation grant WCRF 99A28. The IARC Oral Cancer Multicenter study was funded by grant S06 96 202489 05F02 from Europe against Cancer; grants FIS 97/0024, FIS 97/0662, and BAE 01/5013 from Fondo de Investigaciones Sanitarias, Spain; the UICC Yamagiwa-Yoshida Memorial International Cancer Study; the National Cancer Institute of Canada; Associazione Italiana per la Ricerca sul Cancro; and the Pan-American Health Organization. Coordination of the EPIC study is financially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The lung cancer genome-wide association analyses: Transdisciplinary Research for Cancer in Lung (TRICL) of the International Lung Cancer Consortium (ILCCO) was supported by (U19-CA148127, CA148127S1, U19CA203654, and Cancer Prevention Research Institute of Texas RR170048). The ILCCO data harmonization is supported by Cancer Care Ontario Research Chair of Population Studies to R. H. and Lunenfeld-Tanenbaum Research Institute, Sinai Health System. The TRICL-ILCCO OncoArray was supported by in-kind genotyping by the Centre for Inherited Disease Research (26820120008i-0-26800068-1). The CAPUA study was supported by FIS-FEDER/Spain grant numbers FIS-01/310, FIS-PI03-0365, and FIS-07-BI060604, FICYT/Asturias grant numbers FICYT PB02-67 and FICYT IB09-133, and the University Institute of Oncology (IUOPA), of the University of Oviedo and the Ciber de Epidemiologia y Salud Pública. CIBERESP, SPAIN. The work performed in the CARET study was supported by the National Institute of Health/National Cancer Institute: UM1 CA167462 (PI: Goodman), National Institute of Health UO1-CA6367307 (PIs Omen, Goodman); National Institute of Health R01 CA111703 (PI Chen), National Institute of Health 5R01 CA151989-01A1(PI Doherty). The Liverpool Lung project is supported by the Roy Castle Lung Cancer Foundation. The Harvard Lung Cancer Study was supported by the NIH (National Cancer Institute) grants CA092824, CA090578, CA074386. The Multi-ethnic Cohort Study was partially supported by NIH Grants CA164973, CA033619, CA63464, and CA148127. The work performed in MSH-PMH study was supported by The Canadian Cancer Society Research Institute (020214), Ontario Institute of Cancer and Cancer Care Ontario Chair Award to R.J.H. and G.L. and the Alan Brown Chair and Lusi Wong Programs at the Princess Margaret Hospital Foundation. NJLCS was funded by the State Key Program of National Natural Science of China (81230067), the National Key Basic Research Program Grant (2011CB503805), the Major Program of the National Natural Science Foundation of China (81390543). The Norway study was supported by Norwegian Cancer Society, Norwegian Research Council. The Shanghai Cohort Study (SCS) was supported by National Institutes of Health R01 CA144034 (PI: Yuan) and UM1 CA182876 (PI: Yuan). The Singapore Chinese Health Study (SCHS) was supported by National Institutes of Health R01 CA144034 (PI: Yuan) and UM1 CA182876 (PI: Yuan). The work in TLC study has been supported in part the James & Esther King Biomedical Research Program (09KN-15), National Institutes of Health Specialized Programs of Research Excellence (SPORE) Grant (P50 CA119997), and by a Cancer Center Support Grant (CCSG) at the H. Lee Moffitt Cancer Center and Research Institute, an NCI designated Comprehensive Cancer Center (grant number P30-CA76292). The Vanderbilt Lung Cancer Study—BioVU dataset used for the analyses described was obtained from Vanderbilt University Medical Center's BioVU, which is supported by institutional funding, the 1S10RR025141-01 instrumentation award, and by the Vanderbilt CTSA grant UL1TR000445 from NCATS/NIH. Dr. Aldrich was supported by NIH/National Cancer Institute K07CA172294 (PI: Aldrich) and Dr. Bush was supported by NHGRI/NIH U01HG004798 (PI: Crawford). The Copenhagen General Population Study (CGPS) was supported by the Chief Physician Johan Boserup and Lise Boserup Fund, the Danish Medical Research Council and Herlev Hospital. The NELCS study: Grant Number P20RR018787 from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH). The Kentucky Lung Cancer Research Initiative was supported by the Department of Defense [Congressionally Directed Medical Research Program, U.S. Army Medical Research and Materiel Command Program] under award number: 10153006 (W81XWH-11-1-0781). Views and opinions of, and endorsements by the author(s) do not reflect those of the US Army or the Department of Defense. This research was also supported by unrestricted infrastructure funds from the UK Center for Clinical and Translational Science, NIH grant UL1TR000117 and Markey Cancer Center NCI Cancer Center Support Grant (P30 CA177558) Shared Resource Facilities: Cancer Research Informatics, Biospecimen and Tissue Procurement, and Biostatistics and Bioinformatics. The M.D. Anderson Cancer Center study was supported in part by grants from the NIH (P50 CA070907, R01 CA176568) (to X.W.), Cancer Prevention & Research Institute of Texas (RP130502) (to X.W.), and The University of Texas MD Anderson Cancer Center institutional support for the Center for Translational and Public Health Genomics. The deCODE study of smoking and nicotine dependence was funded in part by a grant from NIDA (R01- DA017932). The study in Lodz center was partially funded by Nofer Institute of Occupational Medicine, under task NIOM 10.13: Predictors of mortality from non-small cell lung cancer—field study. Genetic sharing analysis was funded by NIH grant CA194393. The research undertaken by M.D.T., L.V.W., and M.S.A. was partly funded by the National Institute for Health Research (NIHR). The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health. M.D.T. holds a Medical Research Council Senior Clinical Fellowship (G0902313). The work to assemble the FTND GWAS meta-analysis was supported by the National Institutes of Health (NIH), National Institute on Drug Abuse (NIDA) grant number R01 DA035825 (Principal Investigator [PI]: DBH). The study populations included COGEND (dbGaP phs000092.v1.p1 and phs000404.v1.p1), COPDGene (dbGaP phs000179.v3.p2), deCODE Genetics, EAGLE (dbGaP phs000093.vs.p2), and SAGE. dbGaP phs000092.v1.p1). See Hancock et al. Transl Psychiatry 2015 (PMCID: PMC4930126) for the full listing of funding sources and other acknowledgments. The Resource for the Study of Lung Cancer Epidemiology in North Trent (ReSoLuCENT)study was funded by the Sheffield Hospitals Charity, Sheffield Experimental Cancer Medicine Centre and Weston Park Hospital Cancer Charity. The ovarian cancer genome-wide association analysis: The Ovarian Cancer Association Consortium (OCAC) is supported by a grant from the Ovarian Cancer Research Fund thanks to donations by the family and friends of Kathryn Sladek Smith (PPD/RPCI.07). The scientific development and funding for this project were in part supported by the US National Cancer Institute GAME-ON Post-GWAS Initiative (U19-CA148112). This study made use of data generated by the Wellcome Trust Case Control consortium that was funded by the Wellcome Trust under award 076113. The results published here are in part based upon data generated by The Cancer Genome Atlas Pilot Project established by the National Cancer Institute and National Human Genome Research Institute (dbGap accession number phs000178.v8.p7). The OCAC OncoArray genotyping project was funded through grants from the U.S. National Institutes of Health (CA1X01HG007491-01 (C.I.A.), U19-CA148112 (T.A.S.), R01-CA149429 (C.M.P.), and R01-CA058598 (M.T.G.); Canadian Institutes of Health Research (MOP-86727 (L.E.K.) and the Ovarian Cancer Research Fund (A.B.). The COGS project was funded through a European Commission's Seventh Framework Programme grant (agreement number 223175 - HEALTH-F2-2009-223175) and through a grant from the U.S. National Institutes of Health (R01-CA122443 (E.L.G)). Funding for individual studies: AAS: National Institutes of Health (RO1-CA142081); AOV: The Canadian Institutes for Health Research (MOP-86727); AUS: The Australian Ovarian Cancer Study Group was supported by the U.S. Army Medical Research and Materiel Command (DAMD17-01-1-0729), National Health & Medical Research Council of Australia (199600, 400413 and 400281), Cancer Councils of New South Wales, Victoria, Queensland, South Australia and Tasmania and Cancer Foundation of Western Australia (Multi-State Applications 191, 211, and 182). The Australian Ovarian Cancer Study gratefully acknowledges additional support from Ovarian Cancer Australia and the Peter MacCallum Foundation; BAV: ELAN Funds of the University of Erlangen-Nuremberg; BEL: National Kankerplan; BGS: Breast Cancer Now, Institute of Cancer Research; BVU: Vanderbilt CTSA grant from the National Institutes of Health (NIH)/National Center for Advancing Translational Sciences (NCATS) (ULTR000445); CAM: National Institutes of Health Research Cambridge Biomedical Research Centre and Cancer Research UK Cambridge Cancer Centre; CHA: Innovative Research Team in University (PCSIRT) in China (IRT1076); CNI: Instituto de Salud Carlos III (PI12/01319); Ministerio de Economía y Competitividad (SAF2012); COE: Department of Defense (W81XWH-11-2-0131); CON: National Institutes of Health (R01-CA063678, R01-CA074850; and R01-CA080742); DKE: Ovarian Cancer Research Fund; DOV: National Institutes of Health R01-CA112523 and R01-CA87538; EMC: Dutch Cancer Society (EMC 2014-6699); EPC: The coordination of EPIC is financially supported by the European Commission (DG-SANCO) and the International Agency for Research on Cancer. The national cohorts are supported by Danish Cancer Society (Denmark); Ligue Contre le Cancer, Institut Gustave Roussy, Mutuelle Générale de l'Education Nationale, Institut National de la Santé et de la Recherche Médicale (INSERM) (France); German Cancer Aid, German Cancer Research Center (DKFZ), Federal Ministry of Education and Research (BMBF) (Germany); the Hellenic Health Foundation (Greece); Associazione Italiana per la Ricerca sul Cancro-AIRC-Italy and National Research Council (Italy); Dutch Ministry of Public Health, Welfare and Sports (VWS), Netherlands Cancer Registry (NKR), LK Research Funds, Dutch Prevention Funds, Dutch ZON (Zorg Onderzoek Nederland), World Cancer Research Fund (WCRF), Statistics Netherlands (The Netherlands); ERC-2009-AdG 232997 and Nordforsk, Nordic Centre of Excellence programme on Food, Nutrition and Health (Norway); Health Research Fund (FIS), PI13/00061 to Granada, PI13/01162 to EPIC-Murcia, Regional Governments of Andalucía, Asturias, Basque Country, Murcia and Navarra, ISCIII RETIC (RD06/0020) (Spain); Swedish Cancer Society, Swedish Research Council and County Councils of Skåne and Västerbotten (Sweden); Cancer Research UK (14136 to EPIC-Norfolk; C570/A16491 and C8221/A19170 to EPIC-Oxford), Medical Research Council (1000143 to EPIC-Norfolk, MR/M012190/1 to EPIC-Oxford) (United Kingdom); GER: German Federal Ministry of Education and Research, Programme of Clinical Biomedical Research (01 GB 9401) and the German Cancer Research Center (DKFZ); GRC: This research has been co-financed by the European Union (European Social Fund—ESF) and Greek national funds through the Operational Program "Education and Lifelong Learning" of the National Strategic Reference Framework (NSRF)—Research Funding Program of the General Secretariat for Research & Technology: SYN11_10_19 NBCA. Investing in knowledge society through the European Social Fund; GRR: Roswell Park Cancer Institute Alliance Foundation, P30 CA016056; HAW: U.S. National Institutes of Health (R01-CA58598, N01-CN-55424, and N01-PC-67001); HJO: Intramural funding; Rudolf-Bartling Foundation; HMO: Intramural funding; Rudolf-Bartling Foundation; HOC: Helsinki University Research Fund; HOP: Department of Defense (DAMD17-02-1-0669) and NCI (K07-CA080668, R01-CA95023, P50-CA159981 MO1-RR000056 R01-CA126841); HUO: Intramural funding; Rudolf-Bartling Foundation; JGO: JSPS KAKENHI grant; JPN: Grant-in-Aid for the Third Term Comprehensive 10-Year Strategy for Cancer Control from the Ministry of Health, Labour and Welfare; KRA: This study (Ko-EVE) was supported by a grant from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), and the National R&D Program for Cancer Control, Ministry of Health & Welfare, Republic of Korea (HI16C1127; 0920010); LAX: American Cancer Society Early Detection Professorship (SIOP-06-258-01-COUN) and the National Center for Advancing Translational Sciences (NCATS), Grant UL1TR000124; LUN: ERC-2011-AdG 294576-risk factors cancer, Swedish Cancer Society, Swedish Research Council, Beta Kamprad Foundation; MAC: National Institutes of Health (R01-CA122443, P30-CA15083, P50-CA136393); Mayo Foundation; Minnesota Ovarian Cancer Alliance; Fred C. and Katherine B. Andersen Foundation; Fraternal Order of Eagles; MAL: Funding for this study was provided by research grant R01- CA61107 from the National Cancer Institute, Bethesda, MD, research grant 94 222 52 from the Danish Cancer Society, Copenhagen, Denmark; and the Mermaid I project; MAS: Malaysian Ministry of Higher Education (UM.C/HlR/MOHE/06) and Cancer Research Initiatives Foundation; MAY: National Institutes of Health (R01-CA122443, P30-CA15083, and P50-CA136393); Mayo Foundation; Minnesota Ovarian Cancer Alliance; Fred C. and Katherine B. Andersen Foundation; MCC: Cancer Council Victoria, National Health and Medical Research Council of Australia (NHMRC) grants number 209057, 251533, 396414, and 504715; MDA: DOD Ovarian Cancer Research Program (W81XWH-07-0449); MEC: NIH (CA54281, CA164973, CA63464); MOF: Moffitt Cancer Center, Merck Pharmaceuticals, the state of Florida, Hillsborough County, and the city of Tampa; NCO: National Institutes of Health (R01-CA76016) and the Department of Defense (DAMD17-02-1-0666); NEC: National Institutes of Health R01-CA54419 and P50-CA105009 and Department of Defense W81XWH-10-1-02802; NHS: UM1 CA186107, P01 CA87969, R01 CA49449, R01-CA67262, UM1 CA176726; NJO: National Cancer Institute (NIH-K07 CA095666, R01-CA83918, NIH-K22-CA138563, and P30-CA072720) and the Cancer Institute of New Jersey; If Sara Olson and/or Irene Orlow is a co-author, please add NCI CCSG award (P30-CA008748) to the funding sources; NOR: Helse Vest, The Norwegian Cancer Society, The Research Council of Norway; NTH: Radboud University Medical Centre; OPL: National Health and Medical Research Council (NHMRC) of Australia (APP1025142) and Brisbane Women's Club; ORE: OHSU Foundation; OVA: This work was supported by Canadian Institutes of Health Research grant (MOP-86727) and by NIH/NCI 1 R01CA160669-01A1; PLC: Intramural Research Program of the National Cancer Institute; POC: Pomeranian Medical University; POL: Intramural Research Program of the National Cancer Institute; PVD: Canadian Cancer Society and Cancer Research Society GRePEC Program; RBH: National Health and Medical Research Council of Australia; RMH: Cancer Research UK, Royal Marsden Hospital; RPC: National Institute of Health (P50-CA159981, R01-CA126841); SEA: Cancer Research UK (C490/A10119 C490/A10124); UK National Institute for Health Research Biomedical Research Centres at the University of Cambridge; SIS: NIH, National Institute of Environmental Health Sciences, Z01-ES044005 and Z01-ES049033; SMC: The bbSwedish Research Council-SIMPLER infrastructure; the Swedish Cancer Foundation; SON: National Health Research and Development Program, Health Canada, grant 6613-1415-53; SRO: Cancer Research UK (C536/A13086, C536/A6689) and Imperial Experimental Cancer Research Centre (C1312/A15589); STA: NIH grants U01 CA71966 and U01 CA69417; SWE: Swedish Cancer foundation, WeCanCureCancer and VårKampMotCancer foundation; SWH: NIH (NCI) grant R37-CA070867; TBO: National Institutes of Health (R01-CA106414-A2), American Cancer Society (CRTG-00-196-01-CCE), Department of Defense (DAMD17-98-1-8659), Celma Mastery Ovarian Cancer Foundation; TOR: NIH grants R01-CA063678 and R01 CA063682; UCI: NIH R01-CA058860 and the Lon V Smith Foundation grant LVS39420; UHN: Princess Margaret Cancer Centre Foundation-Bridge for the Cure; UKO: The UKOPS study was funded by The Eve Appeal (The Oak Foundation) and supported by the National Institute for Health Research University College London Hospitals Biomedical Research Centre; UKR: Cancer Research UK (C490/A6187), UK National Institute for Health Research Biomedical Research Centres at the University of Cambridge; USC: P01CA17054, P30CA14089, R01CA61132, N01PC67010, R03CA113148, R03CA115195, N01CN025403, and California Cancer Research Program (00-01389V-20170, 2II0200); VAN: BC Cancer Foundation, VGH & UBC Hospital Foundation; VTL: NIH K05-CA154337; WMH: National Health and Medical Research Council of Australia, Enabling Grants ID 310670 & ID 628903. Cancer Institute NSW Grants 12/RIG/1-17 & 15/RIG/1-16; WOC: National Science Centren (N N301 5645 40). The Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Warsaw, Poland. The University of Cambridge has received salary support for PDPP from the NHS in the East of England through the Clinical Academia Reserve. The prostate cancer genome-wide association analyses: we pay tribute to Brian Henderson, who was a driving force behind the OncoArray project, for his vision and leadership, and who sadly passed away before seeing its fruition. We also thank the individuals who participated in these studies enabling this work. The ELLIPSE/PRACTICAL (http//:practical.icr.ac.uk) prostate cancer consortium and his collaborating partners were supported by multiple funding mechanisms enabling this current work. ELLIPSE/PRACTICAL Genotyping of the OncoArray was funded by the US National Institutes of Health (NIH) (U19 CA148537 for ELucidating Loci Involved in Prostate Cancer SuscEptibility (ELLIPSE) project and X01HG007492 to the Center for Inherited Disease Research (CIDR) under contract number HHSN268201200008I). Additional analytical support was provided by NIH NCI U01 CA188392 (F.R.S.). Funding for the iCOGS infrastructure came from the European Community's Seventh Framework Programme under grant agreement n° 223175 (HEALTH-F2-2009-223175) (COGS), Cancer Research UK (C1287/A10118, C1287/A 10710, C12292/A11174, C1281/A12014, C5047/A8384, C5047/A15007, C5047/A10692, and C8197/A16565), the National Institutes of Health (CA128978) and Post-Cancer GWAS initiative (1U19 CA148537, 1U19 CA148065, and 1U19 CA148112; the GAME-ON initiative), the Department of Defense (W81XWH-10-1-0341), the Canadian Institutes of Health Research (CIHR) for the CIHR Team in Familial Risks of Breast Cancer, Komen Foundation for the Cure, the Breast Cancer Research Foundation, and the Ovarian Cancer Research Fund. This work was supported by the Canadian Institutes of Health Research, European Commission's Seventh Framework Programme grant agreement n° 223175 (HEALTH-F2-2009-223175), Cancer Research UK Grants C5047/A7357, C1287/A10118, C1287/A16563, C5047/A3354, C5047/A10692, C16913/A6135, C5047/A21332 and The National Institute of Health (NIH) Cancer Post-Cancer GWAS initiative grant: No. 1 U19 CA148537-01 (the GAME-ON initiative). We also thank the following for funding support: The Institute of Cancer Research and The Everyman Campaign, The Prostate Cancer Research Foundation, Prostate Research Campaign UK (now Prostate Action), The Orchid Cancer Appeal, The National Cancer Research Network UK, and The National Cancer Research Institute (NCRI) UK. We are grateful for support of NIHR funding to the NIHR Biomedical Research Centre at The Institute of Cancer Research and The Royal Marsden NHS Foundation Trust. The Prostate Cancer Program of Cancer Council Victoria also acknowledge grant support from The National Health and Medical Research Council, Australia (126402, 209057, 251533, 396414, 450104, 504700, 504702, 504715, 623204, 940394, and 614296), VicHealth, Cancer Council Victoria, The Prostate Cancer Foundation of Australia, The Whitten Foundation, PricewaterhouseCoopers, and Tattersall's. E.A.O., D.M.K., and E.M.K. acknowledge the Intramural Program of the National Human Genome Research Institute for their support. The BPC3 was supported by the U.S. National Institutes of Health, National Cancer Institute (cooperative agreements U01-CA98233 to D.J.H., U01-CA98710 to S.M.G., U01-CA98216 to E.R., and U01-CA98758 to B.E.H., and Intramural Research Program of NIH/National Cancer Institute, Division of Cancer Epidemiology and Genetics). CAPS GWAS study was supported by the Swedish Cancer Foundation (grant no 09-0677, 11-484, 12-823), the Cancer Risk Prediction Center (CRisP; www.crispcenter.org), a Linneus Centre (Contract ID 70867902) financed by the Swedish Research Council, Swedish Research Council (grant no K2010-70 × -20430-04-3, 2014-2269). The Hannover Prostate Cancer Study was supported by the Lower Saxonian Cancer Society. PEGASUS was supported by the Intramural Research Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health. RAPPER was supported by the NIHR Manchester Biomedical Research Center, Cancer Research UK (C147/A25254, C1094/A18504) and the EU's 7th Framework Programme Grant/Agreement no 60186. Overall: this research has been conducted using the UK Biobank Resource (application number 16549). NHS is supported by UM1 CA186107 (NHS cohort infrastructure grant), P01 CA87969, and R01 CA49449. NHSII is supported by UM1 CA176726 (NHSII cohort infrastructure grant), and R01-CA67262. A.L.K. is supported by R01 MH107649. We would like to thank the participants and staff of the NHS and NHSII for their valuable contributions as well as the following state cancer registries for their help: AL, AZ, AR, CA, CO, CT, DE, FL, GA, ID, IL, IN, IA, KY, LA, ME, MD, MA, MI, NE, NH, NJ, NY, NC, ND, OH, OK, OR, PA, RI, SC, TN, TX, VA, WA, WY. The authors assume full responsibility for analyses and interpretation of these data. ; Peer Reviewed
