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• W2100039832 abstract "Failure of T cells to protect against cancer is thought to result from lack of antigen recognition, chronic activation, and/or suppression by other cells. Using a mouse sarcoma model, we show that glucose consumption by tumors metabolically restricts T cells, leading to their dampened mTOR activity, glycolytic capacity, and IFN-γ production, thereby allowing tumor progression. We show that enhancing glycolysis in an antigenic regressor tumor is sufficient to override the protective ability of T cells to control tumor growth. We also show that checkpoint blockade antibodies against CTLA-4, PD-1, and PD-L1, which are used clinically, restore glucose in tumor microenvironment, permitting T cell glycolysis and IFN-γ production. Furthermore, we found that blocking PD-L1 directly on tumors dampens glycolysis by inhibiting mTOR activity and decreasing expression of glycolysis enzymes, reflecting a role for PD-L1 in tumor glucose utilization. Our results establish that tumor-imposed metabolic restrictions can mediate T cell hyporesponsiveness during cancer." @default.
• W2100039832 created "2016-06-24" @default.
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• W2100039832 date "2015-09-01" @default.
• W2100039832 modified "2023-10-11" @default.
• W2100039832 title "Metabolic Competition in the Tumor Microenvironment Is a Driver of Cancer Progression" @default.
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• W2100039832 doi "https://doi.org/10.1016/j.cell.2015.08.016" @default.
• W2100039832 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4864363" @default.
• W2100039832 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26321679" @default.
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