Anti-VEGF therapy revived by c-Met inhibition, but is c-Met the answer?
- PMID: 22585992
- PMCID: PMC4512948
- DOI: 10.1158/2159-8290.CD-12-0037
Anti-VEGF therapy revived by c-Met inhibition, but is c-Met the answer?
Abstract
A new study by Sennino and colleagues demonstrates that selective VEGF inhibition via the use of an anti-VEGF antibody is sufficient to increase invasion and metastasis in a c-Met-dependent manner. Anti-VEGF therapy induced tumor hypoxia, hypoxia-inducible factor 1α, and c-Met activation in the RIP-Tag2 model of neuroendocrine pancreatic cancer. Selective c-Met inhibition was sufficient to block these effects, providing a potential mechanism for and solution to overcome increased invasion in the face of anti-VEGF therapy.
©2012 AACR.
Conflict of interest statement
R.A. Brekken received a commercial research grant from Affitech A/S and Imclone Systems and consulted for Peregrine Pharmaceuticals. No potential conflicts of interest were disclosed by the other author.
Comment on
-
Suppression of tumor invasion and metastasis by concurrent inhibition of c-Met and VEGF signaling in pancreatic neuroendocrine tumors.Cancer Discov. 2012 Mar;2(3):270-87. doi: 10.1158/2159-8290.CD-11-0240. Epub 2012 Feb 24. Cancer Discov. 2012. PMID: 22585997 Free PMC article.
References
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Molecular Biology Databases
Miscellaneous
