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In: Canadian Slavonic papers: an interdisciplinary journal devoted to Central and Eastern Europe, Volume 53, Issue 2-4, p. 575-661
ISSN: 2375-2475
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In: Canadian Slavonic papers: an interdisciplinary journal devoted to Central and Eastern Europe, Volume 53, Issue 2-4, p. 575-661
ISSN: 2375-2475
In: Canadian Slavonic papers: an interdisciplinary journal devoted to Central and Eastern Europe, Volume 52, Issue 3-4, p. 427-501
ISSN: 2375-2475
In: Canadian Slavonic papers: an interdisciplinary journal devoted to Central and Eastern Europe, Volume 30, Issue 2, p. 265-304
ISSN: 2375-2475
In: Canadian Slavonic papers: an interdisciplinary journal devoted to Central and Eastern Europe, Volume 27, Issue 4, p. 441-477
ISSN: 2375-2475
In: Canadian Slavonic papers: an interdisciplinary journal devoted to Central and Eastern Europe, Volume 51, Issue 2-3, p. 349-406
ISSN: 2375-2475
In: Canadian Slavonic papers: an interdisciplinary journal devoted to Central and Eastern Europe, Volume 49, Issue 3-4, p. 375-429
ISSN: 2375-2475
In: Canadian Slavonic papers: an interdisciplinary journal devoted to Central and Eastern Europe, Volume 48, Issue 3-4, p. 371-429
ISSN: 2375-2475
In: Canadian Slavonic papers: an interdisciplinary journal devoted to Central and Eastern Europe, Volume 28, Issue 2, p. 205-240
ISSN: 2375-2475
In: American political science review, Volume 106, Issue 2, p. 244-275
ISSN: 0003-0554
Tumors have aberrant proteomes that often do not match their corresponding transcriptome profiles. One possible cause of this discrepancy is the existence of aberrant RNA modification landscapes in the so-called epitranscriptome. Here, we report that human glioma cells undergo DNA methylation-associated epigenetic silencing of NSUN5, a candidate RNA methyltransferase for 5-methylcytosine. In this setting, NSUN5 exhibits tumor-suppressor characteristics in vivo glioma models. We also found that NSUN5 loss generates an unmethylated status at the C3782 position of 28S rRNA that drives an overall depletion of protein synthesis, and leads to the emergence of an adaptive translational program for survival under conditions of cellular stress. Interestingly, NSUN5 epigenetic inactivation also renders these gliomas sensitive to bioactivatable substrates of the stress-related enzyme NQO1. Most importantly, NSUN5 epigenetic inactivation is a hallmark of glioma patients with long-term survival for this otherwise devastating disease. ; This work was supported by a European Research Council (ERC) Advanced Grant under the European Community's Seventh Framework Program (FP7/2007-2013)/ERC Grant Agreement No. 268626—EPINORC project (to M. Esteller), the Ministerio de Economía y Competitividad (MINECO) under Grant No. SAF2014-55000-R (to M. Esteller) and the Instituto de Salud Carlos III (ISCIII), under the FIS PI16/01278 Project (to J. Seoane), the Integrated Project of Excellence no. PIE13/00022 (ONCOPROFILE) (to M. Esteller), CIBER 2016 CB16/12/00312 (CIBERONC) (to M. Esteller), co-financed by the European Development Regional Fund, 'A way to achieve Europe' ERDF, the AGAUR—Catalan Government (Project No. 2009SGR1315 and 2014SGR633) (to M. Esteller), the Cellex Foundation (to M. Esteller), Obra Social "La Caixa" (to M. Esteller), the CERCA Program and the Health and Science Departments of the Catalan Government (Generalitat de Catalunya) (to M. Esteller) and a grant from the National Health and Medical Research Council of Australia (APP1061551, to TP). M.W. Boudreau is a member of the NIH Chemistry-Biology Interface Training Program (T32-GM070421).
BASE
For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale.
BASE
For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types.
BASE