Overcoming molecular mechanisms of resistance to first-generation epidermal growth factor receptor tyrosine kinase inhibitors

Clin Lung Cancer. 2012 Jul;13(4):267-79. doi: 10.1016/j.cllc.2011.09.001. Epub 2011 Dec 9.

Abstract

The epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) gefitinib and erlotinib have provided substantial benefits to patients with advanced non-small cell lung cancer (NSCLC). However resistance to these agents has emerged as a significant clinical issue; most patients who initially respond to treatment eventually experience relapse. The mechanisms underlying gefitinib and erlotinib resistance are multifactorial and several have been described. Clearly there is a need for novel and more effective therapies that can overcome resistance to the currently available TKIs. Several agents are in clinical development, including irreversible EGFR TKIs, inhibitors of the MET pathway, and others. In this review we discuss the various underlying mechanisms of gefitinib and erlotinib resistance and highlight the agents currently in clinical development that may have potential for overcoming this resistance.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / therapeutic use*
  • Carcinoma, Non-Small-Cell Lung / drug therapy*
  • Drug Resistance, Neoplasm / physiology
  • ErbB Receptors / antagonists & inhibitors*
  • Erlotinib Hydrochloride
  • Gefitinib
  • Humans
  • Lung Neoplasms / drug therapy*
  • Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Quinazolines / therapeutic use

Substances

  • Antineoplastic Agents
  • Quinazolines
  • Erlotinib Hydrochloride
  • ErbB Receptors
  • Protein-Tyrosine Kinases
  • Gefitinib