Hormone receptor signaling is critical for normal and tumorigenic growth in ovary, breast, and prostate. Recent studies from our lab and others have shown that known oncogenes, such as c-myc and ErbB2, are involved in androgen receptor signaling in prostate cancer. However, the connectivity between the specific pathways is still poorly defined. The experiments in this research proposal will provide important insight into these interactions through the combined study of conditional mouse models and in vitro cell culture. Specifically, they will determine whether downstream oncogenic effectors can compensate for androgenic signaling in vivo, answer if the androgen receptor itself can act as an oncogene, and elucidate how the androgen receptor regulates its downstream targets to control cellular growth. A clear understanding of the crosstalk between hormone receptors and oncogenic signaling pathways is essential for tumor biology as well as the development of targeted molecular therapies.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
1F32CA113132-01
Application #
6885641
Study Section
Special Emphasis Panel (ZRG1-F09 (20))
Program Officer
Lohrey, Nancy
Project Start
2005-09-01
Project End
2006-08-31
Budget Start
2005-09-01
Budget End
2006-08-31
Support Year
1
Fiscal Year
2005
Total Cost
$48,296
Indirect Cost
Name
University of California Los Angeles
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
092530369
City
Los Angeles
State
CA
Country
United States
Zip Code
90095
King, Jennifer C; Xu, Jin; Wongvipat, John et al. (2009) Cooperativity of TMPRSS2-ERG with PI3-kinase pathway activation in prostate oncogenesis. Nat Genet 41:524-6