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Michael E. Cox, Ph.D.

Senior Scientist, The Prostate Centre at Vancouver General Hospital
Assistant Professor of Surgery, Faculty of Medicine, University of British Columbia

Jack Bell Research Centre
2660 Oak St.
Vancouver, BC
Canada V6H 3Z6
Office: 604 875-4818 or 875-4111 ext. 68369
Fax: 604 875-5654
E-mail: mcox@interchange.ubc.ca


Research Interest

Molecular Mechanisms of Prostate Cancer Progression Prostate cancer is the second leading cause of cancer-related deaths in North American men. The disease follows a predictable pattern of presentation as an androgen-dependent carcinoma that over time acquires androgen-independence. Unfortunately, no effective treatment for hormone-refractory disease has been developed. My lab has two primary focuses: investigating the role of prostatic neuroendocrine (NE) cells as a source of paracrine factors that may facilitate androgen independent tumor growth; and the interactions between androgens and specific growth factor receptors and growth factor binding proteins in the development of androgen independence. The aims of the first focus are to identify the signaling pathways critical for NE differentiation, to profile the genetic characteristics of NE differentiation and to determine the effect of factors produced by prostatic NE cells on disease status. We are identifying factors that promote NE differentiation of prostate cancer cell lines and characterizing the intracellular kinase signaling cascades required for potentiating NE differentiation. We are using genomics approaches to characterize the temporal profile of transcriptional changes that occur in response to the convergence of intracellular signaling events that result in NE differentiation of LNCaP cells. We are also developing systems to measure the effect of NE cell-produced neurotrophic factors on androgen-dependence, metastatic and proliferative characteristics of prostate cancer models. The aim of our second focus is to characterize the role growth factors, such as insulin-like growth factor and epidermal growth factor, play in the development of androgen-independence of tumors. We are interested in characterizing the molecular signaling events responsible for the ability of these factors to provide growth and survival signals in the face of androgen withdrawal, gama-radiation and other cytotoxic stresses. Our guiding philosophy is that by understanding the signaling pathways that regulate NE differentiation and secretion of paracrine factors as well as the ability of carcinoma cells to utilize growth and survival stimuli provided by these and other factors, we will identify molecular targets for development of novel therapies for late stage, androgen-independent prostate tumors.




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