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Exploiting the complex biology of prostate cancer

Since my first day as an undergraduate on the campus of Indiana University in Bloomington, I have felt relaxed and comfortable in an academic setting. I had great reverence for my hometown library, but the university campus life was many levels beyond my childhood impression of a learning environment. In my senior year I did independent research with a real “Indiana Jones” character, a physical anthropology/paleontology professor, who sparked my interest in pursuing graduate studies. As my educational interests evolved I turned toward more fundamental sciences. Eventually I decided to study pharmacology and was accepted into a pharmacology program at the University of Colorado in Boulder. As a first-year graduate student, I became excited about cancer research, and my interests focused on endocrine pharmacology under the mentorship of Dr. Leland W.K. Chung. The possibility of finding a cure for cancer, together with my love of research, was too much to resist. Dr. Chung introduced me to the excitement and discipline of biomedical research, specifically prostate cancer research, and for this I continue to be grateful. During the course of my graduate work Dr. Chung also introduced me to his own mentor, Dr. Donald S. Coffey, who made numerous trips to Boulder to encourage the graduate students. Dr. Coffey's enthusiasm and eloquence also had a profound influence on my decision to pursue a career in science. During my graduate student years there were significant breakthroughs in molecular oncology, including the cloning of transforming genes, i.e., oncogenes. These discoveries pushed me to select an area for post-graduate study that would expose me to these new developments in cancer research. The atmosphere in basic oncology research was electric. I knew I had to learn the molecular biology of cancer, and I wanted to learn from the best in the field. My fellowship ambitions led me to the Imperial Cancer Research Fund (ICRF), London, where I was very fortunate to have been mentored by Drs. Malcolm Parker and Hartmut Land. During that period (1985–1988) the environment at the ICRF was exciting and extraordinarily rich in seminal discoveries in the area of molecular carcinogenesis. As a postdoctoral fellow, I developed the mouse prostate reconstitution model (MPR) for prostate cancer. I used this model to demonstrate oncogene cooperativity (ras + myc) in the development of prostate cancer in vivo. This model continues to have unique applications in prostate cancer research. Importantly, with extraordinary teaching and a supportive environment, I developed a fundamental understanding and appreciation of the power of the techniques of molecular biology to uncover the mysteries of cancer and to develop safe and effective medicines for treating cancer. In 1988, I accepted a position as assistant professor in the Scott Department of Urology at Baylor College of Medicine, Houston, Texas. I also received a secondary appointment in the department of Molecular and Cellular Biology. As with the ICRF, I found Baylor College of Medicine (BCM) to be an extraordinarily rich academic environment that allowed me to pursue my own ideas, and I was ready for the challenge. My first few months at BCM also exposed me directly to the clinical side of medicine. I attended urology grand rounds and learned about the suffering and death from genitourinary cancer. These early experiences and my initial encounters and collaborations with academic clinicians and clinical scientists were very important in re-orientating my research in the direction of translational science. I truly loved basic laboratory research, but I wanted to see a positive impact of my research in the clinic, in my lifetime. I decided to continue my focus on prostate cancer, at least initially. At that time an understanding of prostate cancer at the molecular level was minimal and the treatments, exclusively surgery and radiation therapy, although effective in some cases, were (as they remain) not always effective. At BCM, my first few years of independent research involved exploration of new technologies and gaining information about the effects of specific genes on the development and progression of the prostate cancer phenotype from in vivo mouse model systems (mainly the MPR model). One of the first problems I encountered seems now, in retrospect,