title: IDH1/2 mutations and BCL-2 dependence: an unexpected Chink in AML's armour.
abstract: There is a pressing need to develop novel, mechanism-based therapeutic approaches that can be used to improve therapies for genetically defined tumor subtypes. Chan and colleagues have demonstrated recently that BCL-2 inhibitors can target IDH1/2 mutant cancers through a mutant-specific dependency in metabolic regulation.
authors.affiliation: Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
authors.forename: Elodie
authors.initials: E
authors.lastname: Pronier
authors.affiliation: Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Leukemia Service, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 20, New York, NY 10065, USA. Electronic address: leviner@mskcc.org.
authors.forename: Ross L
authors.initials: RL
authors.lastname: Levine
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D019086:Bridged Bicyclo Compounds, Heterocyclic / Q000494:pharmacology*; D019008:Drug Resistance, Neoplasm / Q000235:genetics*; D006801:Humans; D007521:Isocitrate Dehydrogenase / Q000235:genetics*; D015470:Leukemia, Myeloid, Acute / Q000235:genetics*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000037:antagonists & inhibitors*; D013449:Sulfonamides / Q000494:pharmacology*
chemical_list: D000970:Antineoplastic Agents; D019086:Bridged Bicyclo Compounds, Heterocyclic; D019253:Proto-Oncogene Proteins c-bcl-2; D013449:Sulfonamides; D007521:Isocitrate Dehydrogenase