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Description

4) is not able to rescue mel-32 or gcst-1 defective animals (Fig

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(2019) established that AKT activation by phosphatidylinositol 3,4,5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase (PTEN) deficiency, a direct PI3K antagonist, maintained a refractory state of cells to treatment with cytarabine (Ara-C) and IDA through the improvement of glycolysis in the myeloid lines HL60 and KG1

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