Targeting oncogene dependence and resistance

Cancer Cell. 2003 May;3(5):414-7. doi: 10.1016/s1535-6108(03)00115-6.

Abstract

Our expanding experience with imatinib mesylate provides instructive lessons on the power and pitfalls of targeted therapy. The often impressive initial clinical responses seen with imatinib in a variety of malignancies inevitably give way to the emergence of resistant disease. Recent findings reveal several mechanisms of resistance and suggest ways to overcome them.

Publication types

  • Comment
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Alleles
  • Animals
  • Antineoplastic Agents / therapeutic use
  • Benzamides
  • Cell Line, Tumor
  • Drug Resistance, Neoplasm*
  • Enzyme Inhibitors / therapeutic use
  • Fusion Proteins, bcr-abl / genetics
  • Humans
  • Imatinib Mesylate
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • Mutation
  • Neoplasms / drug therapy
  • Neoplasms / genetics
  • Neoplasms / pathology
  • Oncogenes / genetics*
  • Piperazines / therapeutic use
  • Pyrimidines / therapeutic use

Substances

  • Antineoplastic Agents
  • Benzamides
  • Enzyme Inhibitors
  • Piperazines
  • Pyrimidines
  • Imatinib Mesylate
  • Fusion Proteins, bcr-abl