Gene interactions and pathways from curated databases and text-mining
Mol Oncol 2010, PMID: 20106729

Targeting of VEGF-dependent transendothelial migration of cancer cells by bevacizumab.

Prager, Gerald W; Lackner, Eva-Maria; Krauth, Maria-Theresa; Unseld, Matthias; Poettler, Marina; Laffer, Sylvia; Cerny-Reiterer, Sabine; Lamm, Wolfgang; Kornek, Gabriela V; Binder, Bernd R; Zielinski, Christoph C; Valent, Peter

Cancer progression is often associated with the formation of malignant effusions. Vascular endothelial growth factor (VEGF) is a major regulator of vascular permeability and has been implicated as mediator of tumor progression. We examined the production and secretion of VEGF(165) in various primary cancer cells derived from malignant effusions, and the role of exogenous VEGF(165) as a mediator of effusion formation. VEGF(165) was constantly secreted by all cultured tumor cells in an mTOR-dependent manner, as it was inhibited by the mTOR inhibitor rapamycin. Secreted VEGF(165) showed functional activity by inducing endothelial leakiness and tumor cell-transendothelial migration in vitro, effects which could be reverted by the anti-VEGF antibody bevacizumab. Thus, mTOR inhibitors as well as bevacizumab should be considered as potential agents in cancer patients suffering from malignant effusions.

Diseases/Pathways annotated by Medline MESH: Neoplasms
Document information provided by NCBI PubMed

Text Mining Data

VEGF — mTOR: " VEGF ( 165 ) was constantly secreted by all cultured tumor cells in an mTOR dependent manner, as it was inhibited by the mTOR inhibitor rapamycin "

Manually curated Databases

No curated data.