Bcr-Abl and inhibition of apoptosis in chronic myelogenous leukemia cells

Apoptosis. 2000 Oct;5(4):315-8. doi: 10.1023/a:1009623222534.

Abstract

Chronic myelogenous leukemia (CML) cells are highly resistant to apoptosis induced by chemotherapeutic drugs. The observation that production of Bcr-Abl is the initiating event in CML has focussed attention on the survival signals triggered by this oncogene. A number of signal transducers and transcription factors have been associated with the antiapoptotic phenotype of CML cells, some of which lead to the expression and/or activation of members of the Bcl-2 family of apoptosis modulators, such as Bcl-xL and Bad. In this article, recent advances in understanding the antiapoptotic pathways triggered by Bcr-Abl in CML cells, are discussed.

Publication types

  • Review

MeSH terms

  • Apoptosis / physiology*
  • DNA-Binding Proteins / metabolism
  • Fusion Proteins, bcr-abl / genetics
  • Fusion Proteins, bcr-abl / metabolism*
  • Humans
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / physiopathology*
  • Milk Proteins*
  • STAT5 Transcription Factor
  • Signal Transduction*
  • Trans-Activators / metabolism
  • Tumor Cells, Cultured

Substances

  • DNA-Binding Proteins
  • Milk Proteins
  • STAT5 Transcription Factor
  • Trans-Activators
  • Fusion Proteins, bcr-abl