title: 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.
authors.affiliation: Department of Pharmacology, Division of Surgical Oncology, UT Southwestern Medical Center, Dallas, TX 75390-8593, USA.
authors.forename: Kristi D
authors.initials: KD
authors.lastname: Lynn
authors.forename: Rolf A
authors.initials: RA
authors.lastname: Brekken
mesh_terms: D000813:Anilides / Q000494:pharmacology*; D000818:Animals; D057134:Antibodies, Neutralizing / Q000494:pharmacology*; D006801:Humans; D018358:Neuroendocrine Tumors / Q000188:drug therapy*; D010190:Pancreatic Neoplasms / Q000188:drug therapy*; D019859:Proto-Oncogene Proteins c-met / Q000037:antagonists & inhibitors*; D011725:Pyridines / Q000494:pharmacology*; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors*
chemical_list: D000813:Anilides; D057134:Antibodies, Neutralizing; D011725:Pyridines; D042461:Vascular Endothelial Growth Factor A; C558660:cabozantinib; D019859:Proto-Oncogene Proteins c-met