Tumors are dependent upon new blood vessel formation, or angiogenesis, for expansive growth. Our recent analysis of gene expression led to the identification of several genes in endothelial cells that line tumor blood vessels including GPR116, CD137 and CD276. The products of these genes are of particular interest because they reside on the cell surface and may therefore be directly accessible to blood-borne therapeutics. In an attempt to understand their functional role in angiogenesis, we have begun to generate conditional knockouts for GPR116, CD137 and CD276. Because these genes are also likely to be involved developmental angiogenesis we are generating conditional floxed alleles using cre/flp technology such that the gene can be disrupted specifically in the vessels of adult tissues. By challenging gene disrupted mice with tumors, we hope to determine if any of these genes are critical for tumor angiogenesis. The studies should also allow us to better understand the normal physiological function of these genes.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Investigator-Initiated Intramural Research Projects (ZIA)
Project #
1ZIABC010736-04
Application #
7965582
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
4
Fiscal Year
2009
Total Cost
$263,973
Indirect Cost
Name
National Cancer Institute Division of Basic Sciences
Department
Type
DUNS #
City
State
Country
Zip Code
Yang, Mi Young; Hilton, Mary Beth; Seaman, Steven et al. (2013) Essential regulation of lung surfactant homeostasis by the orphan G protein-coupled receptor GPR116. Cell Rep 3:1457-64