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- W2553667461 abstract "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." @default.
- W2553667461 created "2016-11-30" @default.
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- W2553667461 date "2016-11-01" @default.
- W2553667461 modified "2023-10-11" @default.
- W2553667461 title "Tumor-Induced IL-6 Reprograms Host Metabolism to Suppress Anti-tumor Immunity" @default.
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- W2553667461 doi "https://doi.org/10.1016/j.cmet.2016.10.010" @default.
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