Blood · 2007 · 142 citations · 13 references
MedicineHematologyOncologyApoptosisMolecular OncologyOncogenesApoptosis RegulationCancer ProgressionOncogenic Signaling PathwaysPhosphatidylinositol 3-Kinase-akt PathwayPhosphatidylinositol 3-Kinase-akt SignalingPhosphoinositide 3-Kinase SignalingPhosphoinositide 3-Kinase-akt ActivationPhosphoinositide 3-Kinase-akt SignalingPi3 Kinase-akt SignalingPi3k-akt Signaling Pathway
The phosphoinositide 3-kinase (PI3K/Akt) pathway is activated in acute myelogenous leukemia (AML) and is promising for targeted inhibition. Ninety-two patients with primary AML were analyzed for PI3K/Akt constitutive activation. Fifty percent of the patients presented with constitutive PI3K activation (PI3K (+)). No difference was observed between PI3K (+) and PI3K (-) groups concerning age, sex, white blood cell count, lactate dehydrogenase (LDH) level, bone marrow blast cells, French-American-British (FAB) classification, cytogenetics, RAS or nucleophosmin (NPM) mutations. Slightly more FLT3-ITD was detected in the PI3K (-) group (P = .048). The complete remission rate was similar between the 2 groups. With a median follow-up of 26 months, we observed for PI3K (+) and PI3K (-) patients, respectively, 56% and 33% overall survival (P = .001) and 72% and 41% relapse-free survival (P = .001). Constitutive PI3K/Akt activity is a favorable prognosis factor in AML, even after adjustment for FLT3-ITD, and may confer a particular sensitivity to chemotherapy. A better understanding of the downstream effectors of the PI3K/Akt pathway is needed before targeting in AML.
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Internal tandem duplication of the flt3 gene found in acute myeloid leukemia.
Mitsushige Nakao, S Yokota, Toshiki Iwai et al. · PubMed · 1996 · 1.2K citations
Survival of acute myeloid leukemia cells requires PI3 kinase activation
Qing Xu, Serge-Emile Simpson, Timothy J. Scialla et al. · Blood · 2003 · 474 citations · Full text