Prostate cancer is one of the most common malignancies affecting Western males. The comprehensive understanding of the etiology of this disease is nevertheless, far from being complete. This is due to the complexity of this disease as it has a multitude of genetics and environmental factor that could contribute to its development. Epidemiological date indicates that environmental, hormonal and genetic factors could contribute to the tumorigenesis of prostate cancer. Understanding the risk factors may perhaps provide better understanding of the etiology of the disease. Prostate cancer, like other forms of malignancy, is thought to have development due to the accumulation of stepwise mutations. Genetic polymorphisms of some low penetrance genes such as androgen receptor (AR) could also contribute to the development of prostate cancer. AR mediates the action of androgen, which is important for prostate cell proliferation and differentiation. Mutations and amplifications of the AR are observed in some cases of prostate cancer. Androgen receptor signaling pathway plays a critical role in the regulation of prostate cell growth. Deregulation of AR signaling contributes significantly to the progression of the primary disease to the more sever androgen-refractory prostate cancer, which becomes unresponsive to androgen-ablation therapy. This review focused on multiple aspects of AR function in prostate cancer development and progression which may enhance the understanding of AR targeting therapy being a double-sided sword in the context of tumor microenvironment.
Keywords: prostate cancer, malignancy, androgen receptor, polymorphism
Key words: prostate cancer, malignancy, androgen receptor, polymorphism
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