This is a revised application for renewal of the SPORE in Prostate Cancer at the Robert H. Lurie Comprehensive Cancer Center of Northwestern University and the Cancer Research Center of the University of Chicago. Overall, the reviewers noted that the Program had considerable merit with strengths in the expertise of the investigators, large patient population and an environment highly supportive of the SPORE. We have responded to the comments made by the review committee through extensive revisions and, thus, have further enhanced the program throughout. The major changes can be found in Project 4 where we now focus on animal studies and a clinical trial and in Project 2 where we have eliminated one aim to conduct animal studies. The revised application contains four highly translational research projects: (1) 5a-Reductase Inhibition in Intermittent Androgen Ablation Therapy of Prostate Cancer (Wang &Shevrin), (2) PEDF Regulation of Adipogenesis and Leptin in Prostate Cancer (Crawford, Gapstur and Lee), (3) Radiation-lnducible TNF-alpha Therapy in Prostate Cancer (Weichselbaum &Stadler) and (4) Modulation of Prostate Cancer Cell Motility by the Chemopreventive Agent Genistein (Bergan &Catalona). These projects represent a balanced approach in prostate cancer translational research, including prevention (Project 4), molecular epidemiology (Project 2), management of androgen-sensitive advanced cancer (Project 1), and therapy of local disease (project 3). The leadership of the SPORE emphasizes the highly interactive structures in place for the proposed four cores, that include the Administrative Core, the Specimen Procurement Core, the Biostatistics/Bioinformatics Core, and the Clinical Trials and Advocacy Core. The SPORE also has flexible, yet structured, Developmental Research and Career Development Programs to encourage additional investigators to undertake initiatives in prostate cancer research and to quickly respond to new research opportunities. The Internal and External Advisory Committees evaluate program progress and offer guidance to the SPORE principal investigator and co-principal investigators. We feel that the revised application is significantly improved, and we are grateful to the reviewers for their helpful comments.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Specialized Center (P50)
Project #
5P50CA090386-10
Application #
8444295
Study Section
Special Emphasis Panel (ZCA1-RPRB-M (O1))
Program Officer
Hruszkewycz, Andrew M
Project Start
2001-06-01
Project End
2014-01-31
Budget Start
2013-02-01
Budget End
2014-01-31
Support Year
10
Fiscal Year
2013
Total Cost
$2,150,501
Indirect Cost
$485,667
Name
Northwestern University at Chicago
Department
Urology
Type
Schools of Medicine
DUNS #
005436803
City
Chicago
State
IL
Country
United States
Zip Code
60611
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Loeb, Stacy; Sanda, Martin G; Broyles, Dennis L et al. (2015) The prostate health index selectively identifies clinically significant prostate cancer. J Urol 193:1163-9
Grin, Boris; Loeb, Stacy; Roehl, Kim et al. (2015) A rare 8q24 single nucleotide polymorphism (SNP) predisposes North American men to prostate cancer and possibly more aggressive disease. BJU Int 115:101-5
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Venkatasubramanian, Palamadai N; Brendler, Charles B; Plunkett, Beth A et al. (2014) Periprostatic adipose tissue from obese prostate cancer patients promotes tumor and endothelial cell proliferation: a functional and MR imaging pilot study. Prostate 74:326-35
Adams, Daniel L; Martin, Stuart S; Alpaugh, R Katherine et al. (2014) Circulating giant macrophages as a potential biomarker of solid tumors. Proc Natl Acad Sci U S A 111:3514-9
Ai, J; Pascal, L E; O'Malley, K J et al. (2014) Concomitant loss of EAF2/U19 and Pten synergistically promotes prostate carcinogenesis in the mouse model. Oncogene 33:2286-94
Pavese, Janet M; Ogden, Irene M; Voll, Eric A et al. (2014) Mitogen-activated protein kinase kinase 4 (MAP2K4) promotes human prostate cancer metastasis. PLoS One 9:e102289
Kregel, Steven; Szmulewitz, Russell Z; Vander Griend, Donald J (2014) The pluripotency factor Nanog is directly upregulated by the androgen receptor in prostate cancer cells. Prostate 74:1530-43
Wu, L; Runkle, C; Jin, H-J et al. (2014) CCN3/NOV gene expression in human prostate cancer is directly suppressed by the androgen receptor. Oncogene 33:504-13

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