Anti-VE GF Therapy Revived by c-Met Inhibition, But Is c-Met the Answer?

Kristi D. Lynn, Rolf A. Brekken

Research output: Contribution to journalArticle

3 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)211-213
Number of pages3
JournalCancer discovery
Issue number3
StatePublished - Mar 1 2012


ASJC Scopus subject areas

  • Oncology

Cite this