Abstract

Testosterone plays an important role in promoting the differentiation and stimulation of prostate epi-thelial cells. Adding to the basic physiology of testosterone, several studies led to the dissemination of the historical androgen hypothesis that higher circulating androgen levels promote prostate cancer cell growth and make the tumor more aggressive. Whereas, the prostate saturation model accounted for the androgen sensitivity of testosterone stimulation in the prostate up to a saturation point, which occurred near the level of castration. Testosterone is related to prostate cancer metabolism in a com-plex manner; however, within the reference range, high or normal testosterone levels are expected to maintain benign and malignant prostate cells in a differentiated state. Accumulating evidence has suggested that testosterone replacement therapy (TRT) might prevent the development of prostate cancer and even reduce prostate cancer risk. There is no change in the clinical guidelines to be followed when considering TRT in patients with a history of prostate cancer, but it is necessary for the physician to inform patients of the positive effects of TRT on male health and prostate cancer.

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