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10.1016/j.cmet.2016.10.010 http://scihub22266oqcxt.onion/10.1016/j.cmet.2016.10.010 C5106372!5106372!27829137     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Metab 2016 ; 24 (5): 672-84 Nephropedia Template TP {{tp|p=27829137|t=2016. Tumor-Induced IL-6 Reprograms Host Metabolism to Suppress Anti-tumor Immunity |pdf=|usr=}}{{27829137}} gab.com Text Tumor-Induced IL-6 Reprograms Host Metabolism to Suppress Anti-tumor Immunity JO: Cell Metab http://www.kidney.de/pget.php?&tw=1&pmid=27829137 #FOAvip In patients with cancer, the wasting syndrome, cachexia, is associated with caloric deficiency. Here, we describe tumor-induced alterations of the host metabolic response to caloric deficiency that cause intratumoral immune suppression. In pre-cachectic mice with transplanted colorectal cancer or autochthonous pancreatic ductal adenocarcinoma (PDA), we find that IL-6 reduces the hepatic ketogenic potential through suppression of PPARalpha, the transcriptional master regulator of ketogenesis. When these mice are challenged with caloric deficiency, the resulting relative hypoketonemia triggers a marked rise in glucocorticoid levels. Multiple intratumoral immune pathways are suppressed by this hormonal stress response. Moreover, administering corticosterone to elevate plasma corticosterone to a level that is lower than that occurring in cachectic mice abolishes the response of mouse PDA to an immunotherapy that has advanced to clinical trials. Therefore, tumor-induced IL-6 impairs the ketogenic response to reduced caloric intake, resulting in a systemic metabolic stress response that blocks anti-cancer immunotherapy. Twit Text FOAVip Tumor-Induced IL-6 Reprograms Host Metabolism to Suppress Anti-tumor Immunity ????Cell Metab http://www.kidney.de/pget.php?&tw=1&pmid=27829137 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27829137 #FOAvip English Wikipedia <ref>{{Cite pmid|27829137}}</ref> Tumor-Induced IL-6 Reprograms Host Metabolism to Suppress Anti-tumor Immunity #MMPMID27829137 Flint T; Janowitz T; Connell C; Roberts E; Denton A; Coll A; Jodrell D; Fearon D Cell Metab 2016[Nov]; 24 (5): 672-84 PMID27829137show ga In patients with cancer, the wasting syndrome, cachexia, is associated with caloric deficiency. Here, we describe tumor-induced alterations of the host metabolic response to caloric deficiency that cause intratumoral immune suppression. In pre-cachectic mice with transplanted colorectal cancer or autochthonous pancreatic ductal adenocarcinoma (PDA), we find that IL-6 reduces the hepatic ketogenic potential through suppression of PPARalpha, the transcriptional master regulator of ketogenesis. When these mice are challenged with caloric deficiency, the resulting relative hypoketonemia triggers a marked rise in glucocorticoid levels. Multiple intratumoral immune pathways are suppressed by this hormonal stress response. Moreover, administering corticosterone to elevate plasma corticosterone to a level that is lower than that occurring in cachectic mice abolishes the response of mouse PDA to an immunotherapy that has advanced to clinical trials. Therefore, tumor-induced IL-6 impairs the ketogenic response to reduced caloric intake, resulting in a systemic metabolic stress response that blocks anti-cancer immunotherapy. äTumor-Induced IL-6 Reprograms Host Metabolism to Suppress Anti-tumor I(epmc).pdf DeepDyve Pubget Overpricing