Abstract
Whether mutations in metabolic pathways contribute to the pathogenesis of cancer is controversial.1,2 Cancer cells have long been noted to preferentially metabolize glucose through glycolysis, a discovery that has been translated to the clinic through positron-emission-tomography imaging of 18F-deoxyglucose uptake in tumors. Moreover, recent studies have uncovered recurrent somatic mutations in four genes involved in the metabolism of mitochondrial citrate that either cause or predispose cells to become malignant.In this issue of the Journal, Yan and colleagues3 report that 70% or more of low-grade gliomas bear mutations in one of two NADP+-dependent isocitrate dehydrogenase enzymes (IDH1 and . . .
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