Several molecular etiological pathways have been suggested for prostate cancer. Although androgen transactivation pathways clearly have received the greatest attention, others have been the focus of increasing research activity. Among the most prominent of these additional pathways are vitamin D metabolism, insulin-like growth factor (IGF) signaling pathways, and chemical carcinogenic pathways (Fig. 15.1). Hsing and Devesa39 developed an etiological model that integrates these pathways and incorporates many of the possible risk factors suggested for prostate cancer.39 With the availability in the past decade of polymerase chain reaction technology to study polymorphic variants in genes on a large-scale population basis, epidemiologists and molecular biologists have been afforded an opportunity to begin detailed evaluation of these pathways with special attention to the contribution of polygenic variation in prostate cancer development within and between populations. In the section below,
we overview the state of the art related to understanding the contribution of these pathways to prostate cancer incidence. We have chosen not to review the current state of knowledge regarding polymorphisms in metabolic genes and prostate cancer as we believe this is premature in the absence of any clearly established environmental risk exposure. These have been reviewed by Chen.40 More detailed descriptions of our current understanding of the genes involved in the androgen-activation pathway are provided in the chapters which follow.
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