Research Advances

Mayo Clinic's philosophy that the patient comes first is evident throughout the research programs. Laboratory and clinician scientists work together to move the discoveries of the bench to practical application for patients. This process includes clinical studies that evaluate novel therapies among patients and send data back to researchers for analysis. This analysis may result in further research, and hopefully someday a new drug or diagnostic test might become available.

The Prostate Cancer Program has multidisciplinary teams of basic, clinical and population science investigators at Mayo's sites in Phoenix/Scottsdale, Ariz., Jacksonville, Fla., and Rochester, Minn., working together to advance understanding of the biology and genetics of prostate cancer and to find better ways to prevent, diagnose and treat it.

A number of significant findings have been made through contributions of Prostate Cancer Program members. These advances have been made in the areas of tumor biology, genetics, novel treatments and imaging.

Prostate Cancer Program researchers understand that identifying genes occurring differently in normal and malignant prostate tissue using sophisticated techniques capable of identifying thousands of individual genes and proteins (electronic profiling of expressed sequence tags and DNA microarray chip technology) can result in useful diagnostic and prognostic biomarkers.

Mayo's efforts in this area resulted in discovery of a protein called CRISP-3 that, when found in patient blood, indicates the presence of a tumor. That may lead to a test for the presence of CRISP-3 for use in diagnosis and screening for prostate cancer.

Investigators also confirmed that expression of certain genes such as the tumor suppressor protein PTEN and the cell survival protein Bcl-2 are associated with tumor progression in prostate cancer.

A Mayo team determined that a specific region on chromosome-8 (q24) is amplified in prostate cancer tissues, and this is associated with tumor progression. Another group of researchers found that certain cellular pathways important in the regulation of cellular growth, such as the androgen receptor and the PI3K signaling pathways, play key roles in prostate cancer that does not respond to hormonal therapies. These studies may lead to more effective methods for the detection and prognosis of prostate cancer.

Other research advances, both milestones and small steps forward are made every day. The following are some of the findings made by Prostate Cancer Program researchers in the last year.

Haojie Huang, Ph.D.; Kevin Regan; Zhenkun Lou, Ph.D.; Junjie Chen, Ph.D.; and Donald Tindall, Ph.D.; found that CDK2-dependent phosphorylation of FOXO1 is an apoptotic response to DNA damage. Science. 314(5797):294-7, 2006.

Patrick Burch, M.D., in collaboration with a number of other researchers recently published on quality-of-life and pain in advanced stage prostate cancer. They reported the results of a Southwest Oncology Group randomized trial comparing docetaxel and estramustine to mitoxantrone and prednisone—one of many examples of intra- and inter-institutional collaborations within the Prostate Cancer Program. Journal of Clinical Oncology. 24(18): 2828-2835, 2006.

Eric Bergstralh, M.S.; R. Jeffrey Karnes, M.D.; and Michael Blute, M.D.; along with colleagues, reported the long-Term Outcome After Radical Prostatectomy for Patients With Lymph Node Positive Prostate Cancer in the Prostate Specific Antigen Era Journal of Urology. 178(3 pt 1): 864-871, 2007.

Val Lowe, M.D., reported on the clinical significance of diffusely increased 18F-FDG uptake in the thyroid gland. Journal of Nuclear Medicine. 48(6):896-901. 2007.

John Morris, III, M.D.; Sandra Gendler, Ph.D., and other colleagues, reported that adenovirus-mediated and targeted expression of the sodium iodide symporter (NIS) permits in vivo radioiodide imaging and therapy of pancreatic tumors. Human Gene Therapy 17(6): 661-8, 2006.

Alexander Parker, Ph.D.; Eugene Kwon, M.D.; Dr. Blute; Bradley Leibovich, M.D.; George Vasmatzis, Ph.D.; and John Cheville, M.D.; along with other Mayo researchers, demonstrated high expression levels of survivin protein independently predict a poor outcome for patients who undergo surgery for clear cell renal cell carcinoma. Cancer. 107(1):37-45, 2006.

James Cerhan, M.D., Ph.D.; Dr. Blute; Daniel Schaid, Ph.D.; and Stephen Thibodeau, Ph.D.; along with several other Mayo colleagues, demonstrated that two common chromosome 8q24 variants are associated with increased risk for prostate cancer. Cancer Research. 67(7):2944-2950, 2007.

Drs. Tindall, Schaid, Thibodeau, and Wangou Liu, Ph.D., worked with colleagues to show germline p53AIP1 Mutations disrupting DNA damage-induced apoptosis are associated with prostate cancer susceptibility. Cancer Research. 66(21): 10302-10307, 2006.

Charles Young, Ph.D., and others identified ZNF185 as an actin-cytoskeleton associated growth inhibitory LIM protein in prostate cancer. Oncogene, 26(1):111-22. 2007.

Steven Buskirk, M.D.; Thomas Pisansky, M.D.; Robert Myers, M.D.; Alexander Parker, Ph.D.; Todd Igel, M.D.; and other Mayo researchers evaluated prognostic factors and creation of a prognostic scoring system for salvage radiotherapy in patients whose PSA increase after radical prostatectomy. Journal of Urology. 176(3):985-90, 2006.

Dr. Buskirk and Brian Davis, M.D., Ph.D.; along with colleagues, demonstrated combined prostate brachytherapy and short-term androgen deprivation therapy will work as salvage therapy for locally recurrent prostate cancer after external beam irradiation. Journal of Urology. 176(5):2020-4, 2006.