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10.1158/0008-5472.CAN-16-0608 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-16-0608 C5135644!5135644!27530323     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Res 2016 ; 76 (23): 6778-84 Nephropedia Template TP {{tp|p=27530323|t=2016. Inflammation triggers Zeb1-dependent escape from tumor latency |pdf=|usr=}}{{27530323}} gab.com Text Inflammation triggers Zeb1-dependent escape from tumor latency JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27530323 #FOAvip The emergence of metastatic disease in cancer patients many years or decades after initial successful treatment of primary tumors is well documented but poorly understood at the molecular level. Recent studies have begun exploring the cell-intrinsic programs causing disseminated tumor cells to enter latency and the cellular signals in the surrounding non-permissive tissue microenvironment that maintain the latent state. However, relatively little is known about the mechanisms that enable disseminated tumor cells to escape cancer dormancy or tumor latency. We describe here an in vivo model of solitary metastatic latency in the lung parenchyma. The induction of a localized inflammation in the lungs, initiated by lipopolysaccharide (LPS) treatment, triggers the awakening of these cells, which develop into macroscopic metastases. The escape from latency is dependent on the expression of Zeb1, a key regulator of the epithelial-to-mesenchymal transition (EMT). Furthermore, activation of the EMT program on its own, as orchestrated by Zeb1, is sufficient to incite metastatic outgrowth by causing carcinoma cells to enter stably into a metastasis-initiating cellstate. Twit Text FOAVip Inflammation triggers Zeb1-dependent escape from tumor latency ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27530323 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27530323 #FOAvip English Wikipedia <ref>{{Cite pmid|27530323}}</ref> Inflammation triggers Zeb1-dependent escape from tumor latency #MMPMID27530323 De Cock JM; Shibue T; Dongre A; Keckesova Z; Reinhardt F; Weinberg RA Cancer Res 2016[Dec]; 76 (23): 6778-84 PMID27530323show ga The emergence of metastatic disease in cancer patients many years or decades after initial successful treatment of primary tumors is well documented but poorly understood at the molecular level. Recent studies have begun exploring the cell-intrinsic programs causing disseminated tumor cells to enter latency and the cellular signals in the surrounding non-permissive tissue microenvironment that maintain the latent state. However, relatively little is known about the mechanisms that enable disseminated tumor cells to escape cancer dormancy or tumor latency. We describe here an in vivo model of solitary metastatic latency in the lung parenchyma. The induction of a localized inflammation in the lungs, initiated by lipopolysaccharide (LPS) treatment, triggers the awakening of these cells, which develop into macroscopic metastases. The escape from latency is dependent on the expression of Zeb1, a key regulator of the epithelial-to-mesenchymal transition (EMT). Furthermore, activation of the EMT program on its own, as orchestrated by Zeb1, is sufficient to incite metastatic outgrowth by causing carcinoma cells to enter stably into a metastasis-initiating cellstate. äInflammation triggers Zeb1-dependent escape from tumor latency (epmc).pdf DeepDyve Pubget Overpricing