Restoring cancer's death sentence

Cancer Cell. 2006 Nov;10(5):343-5. doi: 10.1016/j.ccr.2006.10.014.


In this issue of Cancer Cell, two groups present data on the function of an antagonist of BCL-2, ABT-737. Both groups find that expression of MCL-1, an antiapoptotic protein related to BCL-2, is a key determinant of resistance to ABT-737. Lowering MCL-1 levels is an effective adjunct to BCL-2 antagonism, and both groups suggest ways that this might be accomplished practically in a clinical setting. The mechanism by which ABT-737 selectively kills cancer cells is discussed below in the context of these and prior reports of ABT-737's function. Antagonism of BCL-2 is an exciting anticancer strategy that may soon become a clinical reality.

Publication types

  • Comment

MeSH terms

  • Animals
  • Biphenyl Compounds / therapeutic use*
  • Humans
  • Myeloid Cell Leukemia Sequence 1 Protein
  • Neoplasm Proteins / metabolism
  • Neoplasms / drug therapy*
  • Neoplasms / metabolism
  • Nitrophenols / therapeutic use*
  • Piperazines / therapeutic use
  • Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Sulfonamides / therapeutic use*
  • bcl-2 Homologous Antagonist-Killer Protein / metabolism
  • bcl-2-Associated X Protein / metabolism


  • ABT-737
  • Biphenyl Compounds
  • Myeloid Cell Leukemia Sequence 1 Protein
  • Neoplasm Proteins
  • Nitrophenols
  • Piperazines
  • Proto-Oncogene Proteins c-bcl-2
  • Sulfonamides
  • bcl-2 Homologous Antagonist-Killer Protein
  • bcl-2-Associated X Protein