Mechanisms of Disease: Polymorphisms of Androgen Regulatory Genes in the Development of Prostate Cancer

Arun S Singh; Cindy H Chau; Douglas K Price; William D Figg

Disclosures

Nat Clin Pract Urol. 2005;2(2):101-107. 

In This Article

Summary and Introduction

Androgens are of primary importance in the etiology of prostate cancer, and binding of the androgen dihydrotestosterone to the androgen receptor is thought to stimulate prostate growth. It has been proposed that polymorphisms within key androgen regulatory genes may contribute to an individual's risk of developing prostate cancer. Attributing single polymorphisms to complex, late-onset, chronic diseases such as prostate cancer is probably not feasible, but identification of genes that increase risk will contribute to larger-scale multigenic risk assessment. Here, we review the current status of our knowledge of associations between important androgen regulatory gene polymorphisms and prostate cancer risk.

It has been estimated that more than 230,000 men in the US will be diagnosed with prostate cancer in 2004 and about 29,900 men will die from the disease that same year.[1] Androgens—testosterone and dihydrotestosterone (DHT)—are important etiologic factors in prostate cancer that exert their effect through binding to the androgen receptor (AR). In turn, the receptor acts as a transcriptional modifier of a variety of genes by binding to an androgen response element. POLYMORPHIC VARIATIONS have been found in genes involved in the biosynthesis, activation, metabolism, and degradation of androgens. As individualized molecular profiles of prostate cancer will contribute to the development of new preventative and treatment regimens, these polymorphisms have started to receive research attention, albeit only in small, defined populations to date. Here, we briefly describe several of these androgen-related polymorphisms and their putative roles in the development and progression of prostate cancer.

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