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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

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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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The lymphocytes isolated above were subjected to immunofluorescence staining with Rat FITC, APC, PE (BD Pharmingen, USA), and labeled anti-rat CD3 + , CD4 + , and CD8 + monoclonal antibodies, respectively, reacting at 4C for 30 min in the dark