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Prostate cancer (Pca) is the leading malignancy and the 2nd cause of death by cancer in North American men. While localized Pca is curable, extraprostatic spread heralds our therapeutic ability and considerably increases the likehood of death from Pca. Six decades after the discovery and use of endocrine therapies, it has become clear that only the androgen-dependent component of Pca can be controlled by androgen ablation and on a temporary basis. Our research deals with molecular, cellular, and clinical aspects of mechanisms explaining how prostate cancer cells surviving androgen ablation therapy inevitably grow and kill Pca patients. Among others, we are focusing on protein kinases linked to the growth and migration of Pca cells as well as on the paracrine regulation of their activation by neuroendocrine (NE) cell products found in the tumor cell microenvironment. Our studies on similar mechanisms being up-regulated in normal basal/stem cells when induced to grow under androgen deprivation support the contribution of stem cells in Pca. Accordingly, strategies (gene therapies) are being developed to counteract these mechanisms in view of therapeutic applications in Pca. Altogether, it is our firm belief that meaningful advances and discoveries on these mechanisms will lead to the development of new and specific diagnostic tools and therapeutic targets to control selectively the androgen-independent tumor cell subpopulations in Pca.