Journal
CLINICAL CANCER RESEARCH
Volume 19, Issue 7, Pages 1631-1633Publisher
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1078-0432.CCR-13-0051
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Funding
- NINDS NIH HHS [R01 NS059876, R01NS078402, R01 NS078402, R01NS059876] Funding Source: Medline
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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. Clin Cancer Res; 19(7); 1631-3. (C) 2013 AACR.
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