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http://scihub22266oqcxt.onion/ C4496202!4496202!25909160     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2015 ; 6 (11): 9061-72 Nephropedia Template TP {{tp|p=25909160|t=2015. IL-32? suppresses colorectal cancer development via TNFR1-mediated death signaling |pdf=|usr=}}{{25909160}} gab.com Text IL-32 suppresses colorectal cancer development via TNFR1-mediated death signaling JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=25909160 #FOAvip Inflammation is associated with cancer-prone microenvironment, leading to cancer. IL-32 is expressed in chronic inflammation-linked human cancers. To investigate IL-32? in inflammation-linked colorectal carcinogenesis, we generated a strain of mice, expressing IL-32 (IL-32?-Tg). In IL-32?-Tg mice, azoxymethane (AOM)-induced colon cancer incidence was decreased, whereas expression of TNFR1 and TNFR1-medicated apoptosis was increased. Also, IL-32? increased ROS production to induce prolonged JNK activation. In colon cancer patients, IL-32? and TNFR1 were increased. These findings indicate that IL-32? suppressed colon cancer development by promoting the death signaling of TNFR1. Twit Text FOAVip IL-32 suppresses colorectal cancer development via TNFR1-mediated death signaling ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=25909160 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25909160 #FOAvip English Wikipedia <ref>{{Cite pmid|25909160}}</ref> IL-32? suppresses colorectal cancer development via TNFR1-mediated death signaling #MMPMID25909160 Yun HM; Park KR; Kim EC; Han SB; Yoon DY; Hong JT Oncotarget 2015[Apr]; 6 (11): 9061-72 PMID25909160show ga Inflammation is associated with cancer-prone microenvironment, leading to cancer. IL-32 is expressed in chronic inflammation-linked human cancers. To investigate IL-32? in inflammation-linked colorectal carcinogenesis, we generated a strain of mice, expressing IL-32 (IL-32?-Tg). In IL-32?-Tg mice, azoxymethane (AOM)-induced colon cancer incidence was decreased, whereas expression of TNFR1 and TNFR1-medicated apoptosis was increased. Also, IL-32? increased ROS production to induce prolonged JNK activation. In colon cancer patients, IL-32? and TNFR1 were increased. These findings indicate that IL-32? suppressed colon cancer development by promoting the death signaling of TNFR1. äIL-32? suppresses colorectal cancer development via TNFR1-mediated dea(epmc).pdf DeepDyve Pubget Overpricing