FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |   Search Term  Advanced Search

Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe

Previous Volume 360:813-815 February 19, 2009 Number 8 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

	Full Text PDF PDA Full Text Purchase this article Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited E-mail When Letters Appear Related Article by Yan, H. PubMed Citation

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 IDH2). . . . [Full Text of this Article]

Source Information

From the University of Pennsylvania School of Medicine, Philadelphia.

This article has been cited by other articles:

• Benarroch, E. E. (2009). Hypoxia-induced mediators and neurologic disease. Neurology 73: 560-565 [Full Text]  
• Vander Heiden, M. G., Cantley, L. C., Thompson, C. B. (2009). Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation. Science 324: 1029-1033 [Abstract] [Full Text]