Abstract
In 1941, androgen sensitivity of adenocarcinoma of the prostate was demonstrated by Huggins and Hodges (1). The result was a considerable enthusiasm that androgen ablation by surgical orchidectomy or administration of estrogens would treat prostate cancer. Testosterone, a steroidal hormone produced by the testicular tissue, represents the vast majority of circulating androgen. It passes through the prostate-cell membrane, where it is converted to dihydrotestosterone (DHT) by the intracellular enzyme 5 alpha-reductase. DHT is believed to be the intracellular messenger responsible for stimulating the nucleus for protein synthesis after it binds to intracellular receptor (Fig. 1). Bilateral surgical orchidectomy leads to a decrease of the plasma testosterone level from 500 ng/100 mL to about 50 ng/100 mLin the majority of cases.
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Kaisary, A.V. (2009). LH-RH Agonist Role in Prostate Cancer Management. In: Jordan, V.C., Furr, B.J. (eds) Hormone Therapy in Breast and Prostate Cancer. Cancer Drug Discovery and Development. Humana Press. https://doi.org/10.1007/978-1-59259-152-7_17
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DOI: https://doi.org/10.1007/978-1-59259-152-7_17
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