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This article describes the mechanism by which activation of NRF2 promotes KRAS-driven lung carcinogenesis and results in dependence on glutaminolysis, which can be therapeutically exploited

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Consistent with the growth inhibition, cell death significantly increased in BMS-754807 + U0126 treated cells than that in vehicle, BMS-754807, or U0126 treated cells (Fig

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Summary: GF-LR3 is a synthetic analog of insulin-like growth hormone