期刊
ONCOTARGET
卷 6, 期 10, 页码 8062-8070出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.3509
关键词
AML; mTOR signaling; PI3 kinase
资金
- NIH [CA121192, CA77816, CA155566]
- Department of Veterans Affairs [I01-CX000916]
- NIH training grants [T32CA070085, F32CA183536]
The mammalian target of rapamycin (mTOR) and phosphoinositide-3-kinase (PI3K) pathways are often aberrantly activated in acute myeloid leukemia (AML) and play critical roles in proliferation and survival of leukemia cells. We provide evidence that simultaneous targeting of mTOR complexes with the catalytic mTOR inhibitor OSI-027 and of the p110 alpha subunit of PI3K with the specific inhibitor BYL-719 results in efficient suppression of effector pathways and enhanced induction of apoptosis of leukemia cells. Importantly, such a combined targeting approach results in enhanced suppression of primitive leukemic progenitors from patients with AML. Taken together, these findings raise the possibility of combination treatments of mTOR and p110a inhibitors as a unique approach to enhance responses in refractory AML.
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