The Prostate Cancer Program (05) has 3 central themes: 1) mechanisms of castration resistance;2) molecular targeting;and 3) translational studies, both clinical and preclinical. The major program emphasis is on the study of the mechanisms of aberrant androgen receptor (AR) activation in the development of castration resistant prostate cancer (CRPC). Studies to understand the function and regulation of AR divide into 3 areas: a) regulation of intracrine androgens, b) aberrant AR activation, and c) the role of co-regulators. Molecular targeting of CRPC focuses on the role of neuropeptides, kinase inhibitors, and the role of autophagy. In translational studies, eight different targets are under investigation, four of which have progressed to investigator-initiated clinical trials. Our long-term goal is to develop mechanism-based treatments for CRPC and castration-adjunctive therapy that may lead to a more effective intervention than castration alone. The program has 17 members from 8 different departments and divisions. It has 8 NCl-funded projects for $1.1 million ADC (total peer-reviewed funding, $3.1 million ADC). The group has 320 publications;54% are inter-programmatic and 26% are intra-programmatic

Public Health Relevance

Patients die of prostate cancer because the tumors learn to bypass the effects of therapeutic strategies aimed at reducing the supply of androgens to the cancer. This is called castration resistant prostate cancer. The program is aimed at understanding why this occurs, attempting to prevent its occurrence, and developing therapies to treat it once it has occurred.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA093373-11
Application #
8741018
Study Section
Subcommittee G - Education (NCI)
Project Start
2002-07-01
Project End
2016-06-30
Budget Start
2013-07-01
Budget End
2014-06-30
Support Year
11
Fiscal Year
2013
Total Cost
$25,235
Indirect Cost
$8,797
Name
University of California Davis
Department
Type
DUNS #
047120084
City
Davis
State
CA
Country
United States
Zip Code
95618
Zhang, Jin; Lucchesi, Christopher; Chen, Xinbin (2016) A new function for p53 tetramerization domain in cell fate control. Cell Cycle 15:2854-2855
Vinall, Ruth L; Tepper, Clifford G; Ripoll, Alexandra A Z et al. (2016) Decreased expression of let-7c is associated with non-response of muscle-invasive bladder cancer patients to neoadjuvant chemotherapy. Genes Cancer 7:86-97
Kirschbaum, Mark H; Frankel, Paul; Synold, Timothy W et al. (2016) A phase I pharmacodynamic study of GTI-2040, an antisense oligonucleotide against ribonuclotide reductase, in acute leukemias: a California Cancer Consortium study. Leuk Lymphoma 57:2307-14
Taché, Véronique; Bivina, Liga; White, Sophie et al. (2016) Lipoyltransferase 1 Gene Defect Resulting in Fatal Lactic Acidosis in Two Siblings. Case Rep Obstet Gynecol 2016:6520148
Lara, Joshua; Brunson, Ann; Keegan, Theresa H M et al. (2016) Determinants of Survival for Adolescents and Young Adults with Urothelial Bladder Cancer: Results from the California Cancer Registry. J Urol 196:1378-1382
Faisal, Farzana A; Sundi, Debasish; Tosoian, Jeffrey J et al. (2016) Racial Variations in Prostate Cancer Molecular Subtypes and Androgen Receptor Signaling Reflect Anatomic Tumor Location. Eur Urol 70:14-7
Dang, Julie H T; Chen Jr, Moon S (2016) Increasing Hepatitis B Testing and Linkage to Care of Foreign-Born Asians, Sacramento, California, 2012-2013. Public Health Rep 131 Suppl 2:119-24
Rowson-Hodel, Ashley R; Berg, Anastasia L; Wald, Jessica H et al. (2016) Hexamethylene amiloride engages a novel reactive oxygen species- and lysosome-dependent programmed necrotic mechanism to selectively target breast cancer cells. Cancer Lett 375:62-72
Zhao, Yong; Tu, Mei-Juan; Wang, Wei-Peng et al. (2016) Genetically engineered pre-microRNA-34a prodrug suppresses orthotopic osteosarcoma xenograft tumor growth via the induction of apoptosis and cell cycle arrest. Sci Rep 6:26611
Monjazeb, Arta M; Kent, Michael S; Grossenbacher, Steven K et al. (2016) Blocking Indolamine-2,3-Dioxygenase Rebound Immune Suppression Boosts Antitumor Effects of Radio-Immunotherapy in Murine Models and Spontaneous Canine Malignancies. Clin Cancer Res 22:4328-40

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