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D2HG may act as an \u201concometabolite\u201d by inhibiting a class of \u03b1-KG\u2013dependent enzymes involved in epigenetic regulation, collagen synthesis, and cell signaling. Knock-in mouse models of IDH1 mutations have shed light on these mechanisms and will provide valuable animal models for further investigation.<\/jats:p>\n               <jats:p>Significance: Mutations in IDH1 and IDH2 promote the development of a number of malignancies. These active site mutations cause a gain-of-function leading to the accumulation of the rare metabolite D2HG. Mouse models of these mutations should provide insights into the mechanisms driving tumorigenesis and facilitate evaluation of new treatments. Cancer Discov; 3(7); 730\u201341. \u00a92013 AACR.<\/jats:p>","DOI":"10.1158\/2159-8290.cd-13-0083","type":"journal-article","created":{"date-parts":[[2013,6,25]],"date-time":"2013-06-25T03:06:12Z","timestamp":1372129572000},"page":"730-741","update-policy":"https:\/\/doi.org\/10.1158\/crossmark_policy","source":"Crossref","is-referenced-by-count":414,"title":["Oncogenic Isocitrate Dehydrogenase Mutations: Mechanisms, Models, and Clinical Opportunities"],"prefix":"10.1158","volume":"3","author":[{"given":"Rob A.","family":"Cairns","sequence":"first","affiliation":[{"name":"Authors' Affiliations: 1Campbell Family Cancer Research Institute at Princess Margaret Cancer Centre, University Health Network; and 2Departments of Immunology and Medical Biophysics, University of Toronto, Toronto, Ontario, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tak W.","family":"Mak","sequence":"additional","affiliation":[{"name":"Authors' Affiliations: 1Campbell Family Cancer 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