Targeting MET: why, where and how?

Curr Opin Pharmacol. 2013 Aug;13(4):511-8. doi: 10.1016/j.coph.2013.05.018. Epub 2013 Jun 21.

Abstract

Despite the initial skepticism, targeted therapies represent a new perspective in the treatment of cancer. Tyrosine kinases, and in particular receptor tyrosine kinases (RTKs), are considered ideal targets for this type of therapy. MET, the tyrosine kinase receptor for the Hepatocyte Growth Factor (HGF), has recently become a very interesting and studied target in oncology. In this review we discuss firstly 'why' the MET/HGF pathway can be considered a target in human tumors; secondly 'where' MET/HGF inhibition can be useful in cancer treatment and finally 'how' MET and HGF can be inhibited using either monoclonal antibodies or tyrosine kinase inhibitors. We also highlight some questions in the anti-MET/HGF targeted therapy field that are still waiting for an answer.

Publication types

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

MeSH terms

  • Antineoplastic Agents / therapeutic use
  • Humans
  • Neoplasms / drug therapy
  • Neoplasms / metabolism*
  • Proto-Oncogene Proteins c-met / antagonists & inhibitors
  • Proto-Oncogene Proteins c-met / metabolism*

Substances

  • Antineoplastic Agents
  • MET protein, human
  • Proto-Oncogene Proteins c-met