Prostate cancers are initially dependent on the presence of androgens such as testosterone for their ability to grow. The first line of treatment for metastatic prostate cancer is to deprive them of androgens (androgen blockade using drugs to decrease androgen levels). Unfortunately however, with time, these cancers invariably become resistant to this treatment. Our studies of why this occurs have implicated the Bag1L gene product which, in prostate cancers with mutated p53 genes, may sensitize the androgen receptor to very low levels of androgens, permitting the continued growth of these cancers (Nesslinger, Shi, Gumerlock and deVere White, presented at the American Association for Cancer Research meeting, April 2001).

Analysis of alterations in the androgen receptor in prostate cancer is usually laborious and time-consuming. We have developed a rapid method of analysis that involves transferring androgen receptors from prostate cancers into yeast. Our studies can rapidly determine the type of hormone that aberrant androgen receptors respond to, the hormone concentrations to which they are responding, and the presence of mutations in the androgen receptor (Shi, Ma, Kung and deVere White, presented at the American Urologic Association meeting, June 2001).

Department of Urology – Urologic Oncologists

Christopher P. Evans, M.D.
Professor and Chair

Marc Dall'Era, M.D.
Associate Professor and Vice Chair

Stanley A. Yap, M.D., M.Sc., F.R.C.S.C.
Assistant Professor