Killing cancer cells by flipping the Bcl-2/Bax switch

Cancer Cell. 2005 Jul;8(1):5-6. doi: 10.1016/j.ccr.2005.06.012.


Impairment of apoptosis, the physiologic cell death process, is central to cancer development and renders tumors refractory to cytotoxic therapy. Bcl-2, the oncoprotein activated in follicular lymphoma, inhibits the conserved cell death pathway triggered by diverse cytotoxic agents, as do several close relatives. A small-molecule antagonist of these proteins has now been designed by Oltersdorf et al. Strikingly, ABT-737 sensitizes many tumors to cytotoxic agents and is effective as a single agent against certain lymphomas and solid tumors, provoking stable regression in some tumor xenografts. Hence, this work validates Bcl-2-like proteins as important new targets in cancer therapy.

Publication types

  • Review

MeSH terms

  • Apoptosis*
  • Biphenyl Compounds / pharmacology
  • Humans
  • Neoplasms / metabolism
  • Neoplasms / pathology*
  • Nitrophenols
  • Piperazines
  • Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Sulfonamides
  • bcl-2-Associated X Protein


  • ABT-737
  • BAX protein, human
  • Biphenyl Compounds
  • Nitrophenols
  • Piperazines
  • Proto-Oncogene Proteins c-bcl-2
  • Sulfonamides
  • bcl-2-Associated X Protein