Journal
ONCOGENE
Volume 37, Issue 15, Pages 1949-1960Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41388-017-0077-z
Keywords
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Funding
- AMC PhD Scholarship
- Dutch Cancer Society (KWF) [UVA 2014-6839, AMC2016.1-10460]
- National Institutes of Health (Bethesda, MD
- NIH) [R01HL118281, R01HL123904, R01HL132071, R35HL135795]
- AA & MDS International Foundation (Rockville, MD)
- Robert Duggan Charitable Fund (Cleveland, OH)
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Isocitrate dehydrogenase 1 and 2 (IDH1/2) are key enzymes in cellular metabolism, epigenetic regulation, redox states, and DNA repair. IDH1/2 mutations are causal in the development and/or progression of various types of cancer due to supraphysiological production of D-2-hydroxyglutarate. In various tumor types, IDH1/2-mutated cancers predict for improved responses to treatment with irradiation or chemotherapy. The present review discusses the molecular basis of the sensitivity of IDH1/2-mutated cancers with respect to the function of mutated IDH1/2 in cellular processes and their interactions with novel IDH1/2-mutant inhibitors. Finally, lessons learned from IDH1/2 mutations for future clinical applications in IDH1/2 wild-type cancers are discussed.
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