期刊
EXPERIMENTAL HEMATOLOGY
卷 42, 期 4, 页码 247-251出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.exphem.2013.12.001
关键词
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资金
- National Institutes of Health Grant [NIH R21NS074151]
- Leukemia and Lymphoma Society Translational Research Grant [6175-08K23]
The incidence of mutations in isocitrate dehydrogenase 1 and 2 (IDH1/2) in de novo acute myeloid leukemia (AML) is approximately 20%. These mutations result in distinct metabolic characteristics including dependency of cancer cells on glutamine as the main source for alpha-ocketoglutarate, which is consumed by leukemia cells to produce a cancer-derived metabolite, 2-hydroxyglutarate. We sought to exploit this glutamine addiction therapeutically in mutant IDH primary AML cells from patients by measuring cell growth after exposure to a small molecule glutaminase inhibitor, BPTES. We found that BPTES only suppressed the growth of AML cells expressing mutant IDH compared with those expressing wild type IDH. This study lays the groundwork for strategies to target a specific subtype of AML metabolically with IDH mutations with a unique reprogramming of intermediary metabolism that culminates in glutamine dependency of cancer cells for survival. (C) 2014 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc.
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