EGFR-targeted therapies in lung cancer: predictors of response and toxicity

Pharmacogenomics. 2009 Jan;10(1):59-68. doi: 10.2217/14622416.10.1.59.

Abstract

The EGFR pathway has emerged as a key target in non-small-cell lung cancer. EGF receptor (EGFR) inhibition in non-small-cell lung cancer is achieved via small molecular tyrosine kinase inhibitors, such as erlotinib or gefitinib, or monoclonal antibodies such as cetuximab. A growing body of evidence is identifying potential molecular predictors of response and toxicity. This includes tumor-related molecular markers, such as EGFR mutation and copy number, as well as germline markers such as polymorphisms in EGFR or EGFR pathway-related genes. This review focuses on the current state of knowledge of predictors of response and toxicity to EGFR inhibitors in lung cancer.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Antibodies, Monoclonal / adverse effects
  • Antibodies, Monoclonal / pharmacology
  • Antibodies, Monoclonal / therapeutic use*
  • Antineoplastic Agents / adverse effects
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use*
  • Biomarkers, Tumor / analysis
  • Biomarkers, Tumor / genetics
  • Carcinoma, Non-Small-Cell Lung / drug therapy*
  • Carcinoma, Non-Small-Cell Lung / metabolism
  • Carcinoma, Non-Small-Cell Lung / pathology
  • Clinical Trials as Topic
  • Disease-Free Survival
  • ErbB Receptors / antagonists & inhibitors*
  • ErbB Receptors / genetics
  • Humans
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / pathology
  • Polymorphism, Genetic
  • Protein-Tyrosine Kinases / antagonists & inhibitors

Substances

  • Antibodies, Monoclonal
  • Antineoplastic Agents
  • Biomarkers, Tumor
  • EGFR protein, human
  • ErbB Receptors
  • Protein-Tyrosine Kinases