Imatinib resistance and progression of CML to blast crisis: somatic hypermutation AIDing the way

Cancer Cell. 2009 Sep 8;16(3):174-6. doi: 10.1016/j.ccr.2009.08.012.

Abstract

Very little is known about how acquired oncogenic mutations arise. In this issue of Cancer Cell, Klemm and colleagues present evidence supporting a role for the antibody diversification enzyme activation-induced deaminase (AID) in the generation of mutations associated with disease progression and drug resistance in chronic myeloid leukemia.

Publication types

  • Comment

MeSH terms

  • Antineoplastic Agents / therapeutic use
  • Benzamides
  • Blast Crisis / drug therapy*
  • Cell Line, Tumor
  • Cytidine Deaminase / metabolism*
  • Disease Progression
  • Drug Resistance, Neoplasm / genetics*
  • Humans
  • Imatinib Mesylate
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy*
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology
  • Models, Biological
  • Mutation*
  • Piperazines / therapeutic use*
  • Pyrimidines / therapeutic use*

Substances

  • Antineoplastic Agents
  • Benzamides
  • Piperazines
  • Pyrimidines
  • Imatinib Mesylate
  • AICDA (activation-induced cytidine deaminase)
  • Cytidine Deaminase