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Comment
. 2012 Mar;2(3):211-3.
doi: 10.1158/2159-8290.CD-12-0037.

Anti-VEGF therapy revived by c-Met inhibition, but is c-Met the answer?

Kristi D Lynn  1 , Rolf A Brekken
Affiliations
Comment

Anti-VEGF therapy revived by c-Met inhibition, but is c-Met the answer?

Kristi D Lynn et al. Cancer Discov. 2012 Mar.

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.

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Conflict of interest statement

Disclosure of Potential Conflicts of Interest

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.

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