James D. Brooks
Academic Appointments
- Associate Professor, Urology
- Member, Cancer Center
- Member, Bio-X
Contact Information
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Clinical Offices
Uro-Oncology Clinic 875 Blake Wilbur Dr Clinic E Stanford, CA 94305-5826 Tel Work (650) 725-5546 Fax (650) 723-4200Practices at Stanford Hospital and Clinics and Lucile Packard Children's Hospital
Professional Snapshot
Clinical Focus
- Cancer > Urologic Oncology
- Male Cancers - Prostate
- Prostate Cancer
- Nerve-sparing radical prostatectomy
- Prostate Cancer - Urologic Oncology
Administrative Appointments
- Editor-in-Chief, The Open Prostate Cancer Journal (2008 - present)
- Editorial Board, The Prostate (2000 - present)
- Membership Committee, Society for Basic Urologic Research (2004 - present)
Honors and Awards
- Dornier Research Scholar, American Foundation for Urologic Disease (1995-1997)
- Clinician Scientist Award, Doris Duke Foundation (1998-2002)
- Eugene P. Schonfeld Medical Research Award, Kidney Cancer Association (2000-2002)
- Leutje-Stubbs Faculty Scholar, Stanford University School of Medicine (2002-2003)
Professional Education
| Board Recertification: | Urology, American Board of Urology (2009) |
| Board Certification: | Urology, American Board of Urology (2000) |
| Fellowship: | Johns Hopkins University, MD (1997) |
| Residency: | Johns Hopkins University, MD (1994) |
| Residency: | Johns Hopkins University, MD (1990) |
Postdoctoral Advisees
Graduate & Fellowship Program Affiliations
Scientific Focus
Research Interests
We have identified a genetic change common to all human prostate cancer - loss of expression of glutathione S-transferase-pi (GSTP1). Loss of expression is associated with extensive hypermethylation of deoxycytidine residues in 5'-regulatory sequences. Since GSTP1 is involved in defense against carcinogens, we are exploring induction of other carcinogen defense enzymes as a potential prostate cancer prevention strategy. Recently, we have identified several candidate phase 2 enzyme inducing agents that are effective in the prostate. We have used comprehensive gene expression profiling (DNA microarrays) to identify the mechanisms of action of some of these agents, and of other candidate prostate cancer preventive compounds. We have also used gene expression profiling to investigate the transciptional and DNA copy-number changes that occur in prostate and kidney cancer. We are using these large datasets to identify novel diagnostic and prognostic markers for these diseases. We have ongoing projects that correlate gene expression changes with the clinical features of the cancers.
Clinical Trials
Publications
- Prognostic significance of prostate cancer originating from the transition zone. Urol Oncol. 2009 Nov-Dec; (6): 592-7
- Apolipoprotein D (APOD) is a putative biomarker of androgen receptor function in androgen insensitivity syndrome. J Mol Med. 2009; (6): 623-32
- Temporal changes in gene expression induced by sulforaphane in human prostate cancer cells. Prostate. 2009; (2): 181-90
- CD 9 and vimentin distinguish clear cell from chromophobe renal cell carcinoma. BMC Clin Pathol. 2009; (1): 9
- Alteration of gene expression signatures of cortical differentiation and wound response in lethal clear cell renal cell carcinomas. PLoS One. 2009; (6): e6039

