Dr. Tindall holds the position of Director, Vice Chair and Professor of Urologic Research in the Department of Urology at Mayo Clinic in Rochester, Minnesota. Dr. Tindalls research interest is in the area of prostate cancer.
Dr. Tindall currently serves on the editorial boards of several scientific journals (Cancer Prevention Research, Prostate, Associate Editor-Cancer Research, Cancer Letters, Current Cancer Therapy Reviews. Previously, Dr. Tindall has served on the editorial boards of Journal of Andrology (Co-Editor-in-Chief), Endocrinology, The Yearbook of Cancer, and Steroids.
In addition, Dr. Tindall has chaired a number of international conferences. Dr. Tindall has been President of the Society for Basic Urologic Research (1991), Co-Chair of the Prostate Cancer Review Group (sponsored by the National Cancer Institute in 1997), and Chair of the National Cancer Institute Scientific Review Group Subcommittee C-Basic/Preclinical (2003-2004).
Dr. Tindall has published over 220 original scientific papers and has written over 40 reviews and book chapters. He has received several awards, including that from American Men and Women of Science (1978), Men of Achievement (1980), Who's Who in Technology Today (1980), Leading Consultants in Technology (1981) and a Research Career Development Award from National Institutes of Health (1998-1999). 2009-Meritorious Achievement Award of the Society for Basic Urologic Research
Prostate cancer epithelial cells depend on androgens for their survival. Because of this dependence, androgen deprivation therapy is the major treatment of advanced prostate cancer. Such therapy is effective in delaying progression of the disease. However, inevitably with time, the tumors continue to grow. This stage of the disease is referred to as Castration Resistant Prostate Cancer (CRPC). A key question has been how CRPC can survive and then grow in the face of castrate levels of androgens. Dr. Tindalls laboratory has discovered a potential mechanism by which prostate cancer cells survive following androgen deprivation therapy. His laboratory team has shown for the first time that naturally occurring androgen receptor variants can support the expression of many endogenous androgen dependent target genes, as well as the growth of CRPC cells in the absence of androgens. These variants lack the androgen-binding-domain of the receptor protein and are constitutively active. Splice variants increase following androgen depletion and may play an important role in driving proliferation of cells in CRPC. This discovery provides important information to the pharmaceutical industry and may lead to new therapeutics for prostate cancer patients.