Format

Send to

Choose Destination
See comment in PubMed Commons below
Cancer Cell. 2002 Mar;1(2):193-202.

VEGF-A has a critical, nonredundant role in angiogenic switching and pancreatic beta cell carcinogenesis.

Author information

1
Department of Biochemistry & Biophysics, Diabetes and Comprehensive Cancer Centers, University of California at San Francisco, San Francisco, CA 94143, USA.

Abstract

In the RIP1-Tag2 mouse model of pancreatic islet carcinoma, angiogenesis is switched on in a discrete premalignant stage of tumor development, persisting thereafter. Signaling through VEGF receptor tyrosine kinases is a well-established component of angiogenic regulation. We show that five VEGF ligand genes are expressed in normal islets and throughout islet tumorigenesis. To begin dissecting their contributions, we produced an islet beta cell specific knockout of VEGF-A, resulting in islets with reduced vascularity but largely normal physiology. In RIP1-Tag2 mice wherein most oncogene-expressing cells had deleted the VEGF-A gene, both angiogenic switching and tumor growth were severely disrupted, as was the neovasculature. Thus, VEGF-A is crucial for angiogenesis in a prototypical model of carcinogenesis, whose loss is not readily compensated.

PMID:
12086877
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center