Resiliency of lung cancers to EGFR inhibitor treatment unveiled, offering opportunities to divide and conquer EGFR inhibitor resistance

Cancer Discov. 2012 Oct;2(10):872-5. doi: 10.1158/2159-8290.CD-12-0387.

Abstract

The clinical success of EGF receptor (EGFR) inhibitors in patients with lung cancer is limited by the inevitable development of treatment resistance. Two reports in this issue of Cancer Discovery uncover additional mechanisms by which EGFR-mutant lung cancers escape from EGFR kinase inhibitor treatment. These findings pave the way for clinical testing of new rational therapeutic strategies to prevent or overcome resistance to EGFR kinase inhibitors in the clinic.

MeSH terms

  • Cell Line, Tumor
  • Class I Phosphatidylinositol 3-Kinases
  • Drug Resistance, Neoplasm / genetics*
  • ErbB Receptors / antagonists & inhibitors*
  • ErbB Receptors / genetics
  • Erlotinib Hydrochloride
  • Gefitinib
  • Humans
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / genetics*
  • Molecular Targeted Therapy
  • Mutation
  • Phosphatidylinositol 3-Kinases / genetics
  • Protein Kinase Inhibitors / pharmacology
  • Protein Kinase Inhibitors / therapeutic use
  • Quinazolines / therapeutic use
  • Receptor, ErbB-2 / biosynthesis
  • Receptor, ErbB-2 / genetics

Substances

  • Protein Kinase Inhibitors
  • Quinazolines
  • Erlotinib Hydrochloride
  • Phosphatidylinositol 3-Kinases
  • Class I Phosphatidylinositol 3-Kinases
  • PIK3CA protein, human
  • EGFR protein, human
  • ERBB2 protein, human
  • ErbB Receptors
  • Receptor, ErbB-2
  • Gefitinib