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

Overview

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 date

  • March 9, 2015

Research

keywords

  • Antineoplastic Agents
  • Bridged Bicyclo Compounds, Heterocyclic
  • Drug Resistance, Neoplasm
  • Isocitrate Dehydrogenase
  • Leukemia, Myeloid, Acute
  • Proto-Oncogene Proteins c-bcl-2
  • Sulfonamides

Identity

Scopus Document Identifier

  • 84924230465

Digital Object Identifier (DOI)

  • 10.1016/j.ccell.2015.02.013

PubMed ID

  • 25759018

Additional Document Info

volume

  • 27

issue

  • 3