Abstract
Treatment with estrogens is the most commonly used modality for the management of advanced prostatic carcinoma (PCA). Their major mode of action is thought to be by the suppression of Lutenising Hormone (LH) and Follicle Stimulating Hormone (FSH) release from the pituitary to control the output of testosterone (1). Only chloro-trianisene (Tace) does not exert an antigonadotrophic action. The decrease of plasma testosterone and testicular atrophy result primarily from the central gonadotrophin suppression; however, a direct inhibition of testosterone synthesis is also involved (2) (Table 1). There is evidence that estrogens inhibit the testicular
3 β -hydroxysteroid dehydrogenase, thus blocking the degradation of pregnenolone, one step in the formation of testosterone in vivo (3). Since steroidogenesis inhibition requires a high dose of estrogen, this mechanism may only be operative with chlorotrianisene.
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Altwein, J. (1983). Estrogens in the Treatment of Prostatic Cancer. In: Pavone-Macaluso, M., Smith, P.H. (eds) Cancer of the Prostate and Kidney. NATO Advanced Science Institutes Series, vol 53. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-4349-3_39
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DOI: https://doi.org/10.1007/978-1-4684-4349-3_39
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