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Clin Cancer Res. 2013 Apr 1;19(7):1631-3. doi: 10.1158/1078-0432.CCR-13-0051. Epub 2013 Feb 12.

Glioblastoma resistance to anti-VEGF therapy: has the challenge been MET?

Author information

1
Department of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. jhmccarty@mdanderson.org

Abstract

In glioblastoma cells the receptor tyrosine kinase c-Met is upregulated in response to bevacizumab and plays an important role in promoting invasion and tumor recurrence. These data support novel links between VEGF-A and hepatocyte growth factor and suggest that c-Met and its signaling effectors may be effective targets for anti-invasive therapies.

PMID:
23403631
PMCID:
PMC3618531
DOI:
10.1158/1078-0432.CCR-13-0051
[Indexed for MEDLINE]
Free PMC Article
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