The VICC.ORG Investigator Directory

Robert J. Matusik, Ph.D.

William L. Bray Professor of Urologic Surgery
Professor of Cell & Developmental Biology, Cancer Biology
Director of Urologic Surgery Research
VICC Member

Contact Information:

Vanderbilt University Medical Center
A-1302 Medical Center North
Nashville, TN 37232-2765


Robert Matusik is professor of Urologic Surgery, Cancer Biology and Cell & Developmental Biology at Vanderbilt University School of Medicine and director of Urologic Research in the department of Urologic Surgery. He earned his PhD in biochemistry at the University of Rochester in New York in 1976 and completed a post-doctoral fellowship in cell biology at the Baylor College of Medicine in 1979. Matusik joined the faculty of the University of Manitoba (Canada) Department of Physiology in 1979 and grew through the ranks to the position of full professor by the time he left in 1996 to join Vanderbilt?s faculty. He also served as a visit scientist for the British Columbia Cancer Agency, based in Vancouver, from 1992-1993.


Matusik holds numerous research grants from the National Institutes of Health and U.S. Department of Defense to support his research into the genetic, molecular and hormonal factors that contribute to the development and progression of prostate cancer. He also serves as a co-investigator in a Department of Defense grant to support development of a prostate cancer program at Meharry Medical College, a historically black institution in Nashville and a collaborator with Vanderbilt through the Meharry-Vanderbilt Alliance.

A former Damon Runyon-Walter Winchell fellow, Matusik has served on numerous study sections, site visit teams and review committees for the National Institutes of Health, the Department of Defense and the Department of Veterans Affairs. He also served on the editorial board of the journal Molecular Endocrinology.

Research Specialty:

Androgen Regulation of Gene Expression, Transgenic Mouse Models for Prostate Cancer, and Gene Therapy

Research Description:

In North America, one in ten men is diagnosed with prostate cancer. Prostate cancer starts as an androgen dependent disease that progresses to an androgen independent cancer. The androgen independent tumors fail therapy. One of the major impediments to prostate cancer research is that no appropriate animal model system adequately displays the recognized stages of human prostatic disease. Further, no new therapeutic approaches have been developed after current therapy fails. Our laboratory has developed the probasin (PB) gene as a model system for androgen action, to establish new transgenic animal models for prostate cancer, and to test new therapeutic approaches for treatment.

The androgen receptor (AR) can function through similar cis-acting DNA elements similar to the palindromic glucocorticoid response element; however, recent data has shown that distinct AR elements (ARE) exist and function via cooperative interactions of multiple elements in the PB promoter. Further, since the PB promoter directs prostate specific expression in transgenic mice, it has become a model to dissect the key cis-acting DNA elements that control prostate-specific gene expression. Our laboratory has designed new PB promoters that target high levels of transgene expression to the prostate. These new promoters now serve to create new animal models for prostate cancer and to develop gene therapy vectors that will target a therapeutic gene(s) in the treatment of prostate cancer.

The PB promoter has been linked to oncogenes and growth factors to create new transgenic mouse models for prostate cancer. Transgenic mice carrying PB-oncogenes develop various stages of disease including prostatic precursor lesions that advance to an adenocarcinoma and then to high grade metastatic cancer. Gene expression profiles are being analyzed in these animal models to identify the key genes involved in tumor progression. By identifying the genes that are responsible for tumor progression, we can develop new targets for therapeutic intervention. .


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