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Combination therapeutic strategies targeting the TME in cancer The complexity of cancer metabolism is reflected not only in its own metabolic heterogeneity and metabolic adaptability, but also in its interaction with the surrounding environment

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We used our established genetic model in TrC1 prostate cancer cells expressing either AKT1-WT or the clinically relevant activation associated AKT1-E17K mutant and pharmacologic approaches to explore how cancer cell-specific aberrant AKT activation and the activity of AKT-regulated metabolic pathways impact metabolic state and antioxidant defense at the basal state as well as changes in cellular levels of GSH, NADPH, and ROS, short-term and long-term survival upon irradiation

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