EGFR tyrosine kinases inhibitors in cancer treatment: in vitro and in vivo evidence

Front Biosci (Landmark Ed). 2011 Jan 1;16:1962-72. doi: 10.2741/3833.


The increasing understanding of the molecular mechanisms of neoplastic transformation and progression has prompted the search for novel drugs that could interfere with the intracellular targets involved in this process. EGFR is implicated in the development and progression of the majority of the common human epithelial cancer; therefore different agents have been developed to block EGFR activation in cancer cells. This review focuses on EGFR-tyrosine kinase inhibitors in clinical practice that interfere with ATP binding, inhibiting tyrosine kinase activity and subsequently blocking signal transduction from EGFR. We report current knowledge on molecular mechanisms underlying the anticancer activity of EGFR-tyrosine kinase inhibitors in preclinical models, with particular attention to EGFR downstream effectors responsible for treatment efficacy or resistance.

Publication types

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

MeSH terms

  • Antineoplastic Agents / therapeutic use*
  • Apoptosis / drug effects
  • Cell Division / drug effects
  • ErbB Receptors / antagonists & inhibitors
  • ErbB Receptors / physiology
  • Erlotinib Hydrochloride
  • Gefitinib
  • Humans
  • Lapatinib
  • Neoplasm Invasiveness / prevention & control
  • Neoplasm Metastasis / drug therapy
  • Neoplasms / drug therapy*
  • Neovascularization, Pathologic / drug therapy
  • Protein Kinase Inhibitors / therapeutic use*
  • Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Quinazolines / therapeutic use*
  • Signal Transduction / drug effects


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