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

Cancer Discovery
Kristi D Lynn, Rolf A Brekken

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.

References

May 3, 2003·Cancer Cell·Selma PennacchiettiPaolo M Comoglio
Aug 6, 2004·Endocrine Reviews·Napoleone Ferrara
Oct 4, 2006·The Journal of Clinical Investigation·Michael R MancusoDonald M McDonald
Feb 16, 2007·Proceedings of the National Academy of Sciences of the United States of America·Farhad Haghighi RadGeorges Uzan
Jul 20, 2007·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·Henk M W VerheulRoberto Pili
Oct 19, 2007·Proceedings of the National Academy of Sciences of the United States of America·John M L EbosRobert S Kerbel
May 27, 2011·Cancer Research·Weon-Kyoo YouDonald M McDonald
Nov 29, 2011·BMJ : British Medical Journal·Janice Hopkins Tanne

❮ Previous
Next ❯

Citations

Jan 9, 2013·International Journal of Molecular Sciences·Shinya Mizuno, Toshikazu Nakamura
Nov 18, 2017·Endocrine Connections·E T Aristizabal Prada, C J Auernhammer

❮ Previous
Next ❯

Related Concepts

Related Feeds

Arterial-Venous in Development & Disease

Arterial-venous development may play a crucial role in cardiovascular diseases. Here is the latest research.