Format

Send to:

Choose Destination
See comment in PubMed Commons below
J Clin Oncol. 2013 Mar 10;31(8):1089-96. doi: 10.1200/JCO.2012.43.9422. Epub 2013 Feb 11.

MET as a possible target for non-small-cell lung cancer.

Author information

  • 1University of Chicago, Chicago, IL, USA.

Abstract

Lung cancer is a heterogeneous group of disorders that is now being subdivided into molecular subtypes with dedicated targeted therapies. The MET receptor tyrosine kinase has been identified as aberrantly overexpressed, potentially having activating mutations, and amplified in certain subsets of lung cancers. The ligand hepatocyte growth factor (HGF) can also be overexpressed in lung cancer or expressed in stroma, and both the MET receptor and the HGF ligand can be targets for therapeutics, especially in lung cancer. Activation of MET leads to a plethora of biochemical and biologic changes both in normal and cancerous cells. Preclinically, it has been shown that silencing or inactivating MET leads to decreased viability of cancer cells. There are a number of compounds against MET/HGF in clinical trials that have been shown to be active in lung cancers. This review will summarize the biology of MET as well as its therapeutic inhibition in lung cancer.

PMID:
23401458
[PubMed - indexed for MEDLINE]
PMCID:
PMC3589702
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Write to the Help Desk