The Pacific Northwest Prostate Cancer SPORE is a coordinated effort of four institutions with strong programs in prostate cancer research and career development: 1) the Fred Hutchinson Cancer Research Center (FHCRC); 2) the University of Washington (UW) and its affiliated institutions; 3) the Institute for Systems Biology (ISB); and 4) the University of British Columbia and the Prostate Center & Institute of Vancouver General Hospital. These three Seattle-based and the British Columbia (BC)-based institutions have a large number of investigators and laboratories dedicated to prostate cancer (CAP) research. Within this milieu, there already exists substantial technical infrastructure (e.g., genomics), strong multidisciplinary expertise (e.g., molecular biology, biochemistry, epidemiology, genetics, medical & radiation oncology, urology), and extensive resources (e.g., serum, DNA & tissue banks, CaP animal model facilities, CaP genomic arrays, and a CaP clinical trials organization). All four institutions have, and are in the process of generating, increasing resources for programs in translational CaP research and are committed to contributing significant resources toward the goals of this SPORE. The purpose of the SPORE is not only to perform the research projects proposed, but in a larger sense to form the """"""""central supporting piece"""""""" to a large developing """"""""mosaic"""""""" of coordinated translational CaP research in the Pacific Northwest. We believe the projects to be innovative and translational. Project 1 is a population-based study evaluating specific genetic polymorphisms in relation to CaP progression/mortality. Project 2 aims to characterize molecular alterations (karyotype, transcript) of disseminated CaP cells in the context of influencing the clinical management of patients as diagnostic and prognostic indicators. Project 3 will identify critical determinants of the transition from androgen-dependent to androgen-independent CaP, and will validate these findings in well-characterized pre-clinical models and clinical trials. Project 4 seeks to expand our already extensive work on the genomics of CaP and will determine if tumor gene expression profiles can predict the course of disease and response to cytotoxic chemotherapy. We have proposed five Cores in support of these projects (Administration, Specimen/Tissue, Biostatistics, Informatics & Gene Expression, and Clinical Research). The Career Development and Pilot Project Programs we propose will significantly embellish and strengthen the translational orientation of our prostate cancer research and expand opportunities for new investigators.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Specialized Center (P50)
Project #
5P50CA097186-03
Application #
6758022
Study Section
Special Emphasis Panel (ZCA1-GRB-V (M1))
Program Officer
Hruszkewycz, Andrew M
Project Start
2002-09-19
Project End
2007-04-30
Budget Start
2004-05-01
Budget End
2005-04-30
Support Year
3
Fiscal Year
2004
Total Cost
$2,524,662
Indirect Cost
Name
Fred Hutchinson Cancer Research Center
Department
Type
DUNS #
078200995
City
Seattle
State
WA
Country
United States
Zip Code
98109
Barnard, Monique; Quanson, Jonathan L; Mostaghel, Elahe et al. (2018) 11-Oxygenated androgen precursors are the preferred substrates for aldo-keto reductase 1C3 (AKR1C3): Implications for castration resistant prostate cancer. J Steroid Biochem Mol Biol 183:192-201
Ganaie, Arsheed A; Beigh, Firdous H; Astone, Matteo et al. (2018) BMI1 Drives Metastasis of Prostate Cancer in Caucasian and African-American Men and Is A Potential Therapeutic Target: Hypothesis Tested in Race-specific Models. Clin Cancer Res 24:6421-6432
Schweizer, Michael T; Haugk, Kathleen; McKiernan, Jožefa S et al. (2018) A phase I study of niclosamide in combination with enzalutamide in men with castration-resistant prostate cancer. PLoS One 13:e0198389
Peacock, James W; Takeuchi, Ario; Hayashi, Norihiro et al. (2018) SEMA3C drives cancer growth by transactivating multiple receptor tyrosine kinases via Plexin B1. EMBO Mol Med 10:219-238
Pollan, Sara G; Huang, Fangjin; Sperger, Jamie M et al. (2018) Regulation of inside-out ?1-integrin activation by CDCP1. Oncogene 37:2817-2836
Wu, Yi-Mi; Cie?lik, Marcin; Lonigro, Robert J et al. (2018) Inactivation of CDK12 Delineates a Distinct Immunogenic Class of Advanced Prostate Cancer. Cell 173:1770-1782.e14
Schweizer, Michael T; Hancock, Michael L; Getzenberg, Robert H et al. (2018) Hormone levels following surgical and medical castration: defining optimal androgen suppression. Asian J Androl 20:405-406
Yan, Qingxiang; Bantis, Leonidas E; Stanford, Janet L et al. (2018) Combining multiple biomarkers linearly to maximize the partial area under the ROC curve. Stat Med 37:627-642
Lam, Hung-Ming; Nguyen, Holly M; Corey, Eva (2018) Generation of Prostate Cancer Patient-Derived Xenografts to Investigate Mechanisms of Novel Treatments and Treatment Resistance. Methods Mol Biol 1786:1-27
Lam, Hung-Ming; Corey, Eva (2018) Supraphysiological Testosterone Therapy as Treatment for Castration-Resistant Prostate Cancer. Front Oncol 8:167

Showing the most recent 10 out of 400 publications