Suchergebnisse

Dong Zhou, Quan-Xing Liu, Xu-Feng Deng, Hong Zheng, Xiao Lu, Ji-Gang Dai, Li Jiang Department of Thoracic Surgery, Xinqiao Hospital, Third Military Medical University, Chongqing, People's Republic of China Purpose: Anastomotic leakage is the most feared postoperative complication after esophagectomy. Omentoplasty, wrapping the omentum around the alimentary tract anastomosis, is thought to decrease the anastomotic leakage rate. The purpose of this clinical study is to investigate the use of omentoplasty to reinforce cervical esophagogastrostomy after minimally invasive esophagectomy (MIE).Patients and methods: In this retrospective study, the data of 160 consecutive patients who underwent cervical esophagogastrostomy after MIE between September 2012 and May 2015 were analyzed, 87 who underwent omentoplasty (group A) and 73 who did not undergo omentoplasty (group B). The primary outcome was the incidence of anastomotic leakage and anastomotic strictures after the operation. Secondary outcomes were other complications and mortality rate. Univariate and multivariate analysis of variables associated with an increased risk for anastomotic leak was performed.Results: The median age was 61 years (range, 37–82 years). The anastomotic leakage rates were 4.6% (4/87) in group A and 15.1% (11/73) in group B (P = 0.023). There was no statistical significance in anastomotic stricture rates between group A (6.9%) and group B (9.6%; P = 0.535). No difference was noted in other complications between the groups. There was a trend toward lower leak-associated mortality rates for group A (0%) compared with that for group B (4.1%).Conclusion: Cervical esophagogastrostomy with omentoplasty is more effective than esophagogastrostomy without omentoplasty for the prevention of anastomotic leakage in MIE with cervical anastomosis. Omentoplasty could be used as an adjunct technique to reduce the incidence of anastomotic leakage in cervical esophagogastrostomy following MIE. Keywords: omentoplasty, cervical esophagogastrostomy, minimally invasive esophagectomy, anastomosis leakage, stricture

Xiao Lu,1,* Dong Zhou,1,* Bing Hou,1 Quan-Xing Liu,1 Qian Chen,2 Xu-Feng Deng,1,3 Zu-Bin Yu,1 Ji-Gang Dai,1 Hong Zheng1 1Department of Thoracic Surgery, Xinqiao Hospital, Third Military Medical University, Chongqing, People's Republic of China; 2Institute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, People's Republic of China; 3Department of Cardiothoracic Surgery, First People's Hospital of Zunyi, Guizhou, People's Republic of China *These authors contributed equally to this work Background: Chemotherapy is still the primary adjuvant strategy of cancer therapy; however, the emergence of multi-drug resistance has been a cause for concern. Autophagy has been demonstrated to have a protective role against chemotherapeutic drugs in cancer cells, and autophagy inhibition is generally considered to be a promising therapeutic strategy. However, the paucity of effective and specific autophagy inhibitors limits its application. Purpose: The objective of this study was to explore the effect of DCA, small molecular antitumor agent, on the autophagy regulation and chemosensitization in NSCLC cells. Methods: We investigated the autophagy regulation of dichloroacetate (DCA) by laser confocal microscopy and western blotting in A549 and H1975 cell lines. The MTT assay and flow cytometry was performed for explore the chemosensitization effectiveness of DCA. The results were verified with subcutaneous tumor model in nude mice and the immunohistochemistry was applied for assessing the level of cell apoptosis and autophagy in vivo post treatment. Results: We found that DCA, which exhibited antitumor properties in various carcinoma models, induced apoptosis of non-small cell lung cancer cells (NSCLC) by inhibiting cancer cell autophagy. Furthermore, Perifosine, an AKT inhibitor, can greatly weaken the capacity of inducing apoptosis by DCA. The results indicate that the AKT-mTOR pathway, a main negative regulator of autophagy, is involved in the DCA-induced inhibition of autophagy. Then, we detected the effectiveness of autophagy inhibition by DCA. When used in co-treatment with the chemotherapeutic drug paclitaxel (PTX), DCA markedly decreased cell autophagy, enhanced apoptosis and inhibited proliferation in A549 and H1975 cells. The results of the xenograft experiment demonstrate that co-treatment of PTX and DCA can significantly decrease cell proliferation in vivo and prolong the survival of mice. Conclusion: Our results suggest that DCA can inhibit cell autophagy induced by chemotherapeutics, providing a new avenue for cancer chemotherapy sensitization. Keywords: DCA, autophagy, multi-drug resistance, non-small-cell lung cancer, paclitaxel, xenograft nude mice, chemosensitization