Mechanisms of drug resistance in kinases

Expert Opin Investig Drugs. 2011 Feb;20(2):153-208. doi: 10.1517/13543784.2011.546344.

Abstract

Introduction: because of their important roles in disease and excellent 'druggability', kinases have become the second largest drug target family. The great success of the BCR-ABL inhibitor imatinib in treating chronic myelogenous leukemia illustrates the high potential of kinase inhibitor (KI) therapeutics, but also unveils a major limitation: the development of drug resistance. This is a significant concern as KIs reach large patient populations for an expanding array of indications.

Areas covered: we provide an up-to-date understanding of the mechanisms through which KIs function and through which cells can become KI-resistant. We review current and future approaches to overcome KI resistance, focusing on currently approved KIs and KIs in clinical trials. We then discuss approaches to improve KI efficacy and overcome drug resistance and novel approaches to develop less drug resistance-prone KI therapeutics.

Expert opinion: although drug resistance is a concern for current KI therapeutics, recent progress in our understanding of the underlying mechanisms and promising technological advances may overcome this limitation and provide powerful new therapeutics.

Publication types

  • Review

MeSH terms

  • Antineoplastic Agents / therapeutic use*
  • Antineoplastic Combined Chemotherapy Protocols / therapeutic use
  • Clinical Trials as Topic
  • Drug Resistance, Neoplasm*
  • Fusion Proteins, bcr-abl / antagonists & inhibitors
  • Humans
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy*
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive / physiopathology
  • Molecular Targeted Therapy*
  • Mutation, Missense*
  • Protein Kinase Inhibitors / therapeutic use*
  • Protein Kinases / genetics
  • Protein Kinases / metabolism*
  • Stereoisomerism

Substances

  • Antineoplastic Agents
  • Protein Kinase Inhibitors
  • Protein Kinases
  • Fusion Proteins, bcr-abl