title: Glioblastoma resistance to anti-VEGF therapy: has the challenge been MET?
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.
authors: Department of Cancer Biology, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. jhmccarty@mdanderson.org
authors: Joseph H
authors: JH
authors: McCarty
mesh_terms: D020533:Angiogenesis Inhibitors / Q000494:pharmacology*; D000818:Animals; D019008:Drug Resistance, Neoplasm; D006801:Humans; D009389:Neovascularization, Pathologic / Q000235:genetics*; D019859:Proto-Oncogene Proteins c-met / Q000235:genetics* / Q000378:metabolism*; D059467:Transcriptome
chemical_list: D020533:Angiogenesis Inhibitors; D019859:Proto-Oncogene Proteins c-met
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