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In summary, our data demonstrate that increased radioresistance of cancer cells expressing the clinically relevant activation-associated AKT mutant protein AKT-E17K involves multiple metabolic mechanisms: On the one hand, AKT-E17K promoted increased glycolytic activity at basal state and improved the capability of the cells for activating compensatory glycolysis upon irradiation

doi: 10.1515/revneuro-2017-0063, 104 RosenzweigN.Dvir-SzternfeldR.Tsitsou-KampeliA.Keren-ShaulH.Ben-YehudaH.Weill-RaynalP.et al

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Specific Adverse Effects Reported in Clinical Trials While the overall safety profile was excellent, clinical trials documented all adverse events regardless of severity or causality

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