IDH1/2 mutations and BCL-2 dependence: an unexpected Chink in AML's armour

Elodie Pronier; Ross L Levine

doi:10.1016/j.ccell.2015.02.013

IDH1/2 mutations and BCL-2 dependence: an unexpected Chink in AML's armour

Cancer Cell. 2015 Mar 9;27(3):323-5. doi: 10.1016/j.ccell.2015.02.013.

Authors

Elodie Pronier¹, Ross L Levine²

Affiliations

¹ Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
² 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: [email protected].

PMID: 25759018
DOI: 10.1016/j.ccell.2015.02.013

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.

Publication types

Comment

MeSH terms

Antineoplastic Agents / pharmacology*
Bridged Bicyclo Compounds, Heterocyclic / pharmacology*
Drug Resistance, Neoplasm / genetics*
Humans
Isocitrate Dehydrogenase / genetics*
Leukemia, Myeloid, Acute / genetics*
Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors*
Sulfonamides / pharmacology*

Substances

Antineoplastic Agents
Bridged Bicyclo Compounds, Heterocyclic
Proto-Oncogene Proteins c-bcl-2
Sulfonamides
Isocitrate Dehydrogenase