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10.1158/1078-0432.CCR-15-0780 http://scihub22266oqcxt.onion/10.1158/1078-0432.CCR-15-0780 C4818680!4818680!26655845     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26655845&cmd=llinks): Failed to open stream: HTTP request failed! 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Severe hepatitis promotes hepatocellular carcinoma recurrence via NF-?B pathway-mediated epithelial-mesenchymal transition after resection |pdf=|usr=}}{{26655845}} gab.com Text Severe hepatitis promotes hepatocellular carcinoma recurrence via NF- B pathway-mediated epithelial-mesenchymal transition after resection JO: Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26655845 #FOAvip Purpose: Surgical resection is considered as a curative treatment modality for hepatocellular carcinoma (HCC); however, the incidence of postoperative tumor recurrence is high, leading to worse patient survival. Persistent hepatitis (inflammation) is one of risk factors of tumor recurrence after surgical resection. The aim of this study is to investigate the underlying mechanisms linking liver inflammation to HCC progression. Experimental Design: In this study, we used a cytokine array to identify important cytokines whose levels are increased in liver microenvironment with severe hepatitis. We evaluated the morphological changes, migration and invasion ability, and signal transduction in HCC cells with or without inflammatory cytokine in vitro. Finally, we analyzed the NF-?B signal pathway in tumor specimens from 232 patients with HCC by immunohistochemical staining. Results: The pro-inflammatory cytokine TNF-? was increased in the peritumoral microenvironment and contributed to tumor recurrence and metastasis. Specifically, TNF-? promoted HCC cancer cell migration, invasion, and epithelial?mesenchymal transition (EMT) by upregulating the transcriptional regulator, Snail. We identified Snail as a direct target gene downstream of the TNF-?-mediated canonical NF-?B activation. In addition, tumor recurrence-free survival of HCC patients correlated negatively with high p65 and Snail expression and positively with high E-cadherin expression. Conclusion: Our results establish a signaling axis that explains how inflammatory tumor microenvironment promotes HCC recurrence and metastasis. These findings suggest that controlling liver inflammation and/or targeting NF-?B?mediated Snail expression may be a potential therapeutic strategy to prevent HCC recurrence after hepatectomy. Twit Text FOAVip Severe hepatitis promotes hepatocellular carcinoma recurrence via NF- B pathway-mediated epithelial-mesenchymal transition after resection ????Clin Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26655845 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26655845 #FOAvip English Wikipedia <ref>{{Cite pmid|26655845}}</ref> Severe hepatitis promotes hepatocellular carcinoma recurrence via NF-?B pathway-mediated epithelial-mesenchymal transition after resection #MMPMID26655845 Wu TJ; Chang SS; Li CW; Hsu YH; Chen TC; Lee WC; Yeh CT; Hung MC Clin Cancer Res 2016[Apr]; 22 (7): 1800-12 PMID26655845show ga Purpose: Surgical resection is considered as a curative treatment modality for hepatocellular carcinoma (HCC); however, the incidence of postoperative tumor recurrence is high, leading to worse patient survival. Persistent hepatitis (inflammation) is one of risk factors of tumor recurrence after surgical resection. The aim of this study is to investigate the underlying mechanisms linking liver inflammation to HCC progression. Experimental Design: In this study, we used a cytokine array to identify important cytokines whose levels are increased in liver microenvironment with severe hepatitis. We evaluated the morphological changes, migration and invasion ability, and signal transduction in HCC cells with or without inflammatory cytokine in vitro. Finally, we analyzed the NF-?B signal pathway in tumor specimens from 232 patients with HCC by immunohistochemical staining. Results: The pro-inflammatory cytokine TNF-? was increased in the peritumoral microenvironment and contributed to tumor recurrence and metastasis. Specifically, TNF-? promoted HCC cancer cell migration, invasion, and epithelial?mesenchymal transition (EMT) by upregulating the transcriptional regulator, Snail. We identified Snail as a direct target gene downstream of the TNF-?-mediated canonical NF-?B activation. In addition, tumor recurrence-free survival of HCC patients correlated negatively with high p65 and Snail expression and positively with high E-cadherin expression. Conclusion: Our results establish a signaling axis that explains how inflammatory tumor microenvironment promotes HCC recurrence and metastasis. These findings suggest that controlling liver inflammation and/or targeting NF-?B?mediated Snail expression may be a potential therapeutic strategy to prevent HCC recurrence after hepatectomy. äSevere hepatitis promotes hepatocellular carcinoma recurrence via NF-?(epmc).pdf DeepDyve Pubget Overpricing