Glioblastoma resistance to anti-VEGF therapy: has the challenge been MET?
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 23403631.
- Also identified by DOI 10.1158/1078-0432.CCR-13-0051 and PMC identifier 3618531.
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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.
Medical subject headings
- Angiogenesis Inhibitors
- Drug Resistance, Neoplasm
- Neovascularization, Pathologic
- Proto-Oncogene Proteins c-met
- Transcriptome