title: [Hormonotherapy for prostate cancer].
abstract: Since the report by Dr. Huggins, the Nobel prize winner, hormonotherapy has been a predominant treatment modality for prostate cancer for decades around the world because of its anti-cancer effect and simplicity. In the 1960's, the Veterans Administration Co-operative Urological Research Group (VA CURG) in the U.S.A. claimed that synthetic estrogen had significant adverse effects such as cardio-vascular complications, which dissipated the merits of estrogen. They reported that a group of prostate cancer patients who underwent estrogen therapy showed the same survival as a no treatment group. The normal prostate gland is dependent on androgen for its development, growth and function as well as prostate cancer. Ninety to 95% of androgens are synthesized in testicular Leydig cells under the control of the pituitary-gonadal axis, and the remaining androgens come from the adrenal glands. At any point along the axis from the hypothalamus to the prostate cell nuclei, androgen action on the prostate gland can be inhibited. Castration eliminates Leydig cells and estrogen reduces the serum testosterone level by negative feedback to the pituitary gland. Because of the significant side effects of estrogen and the mental injury brought about by castration, LH-RH analogue could have received great popularity. But impotence is still a major consequence of this drug. For less invasive and more economical treatment modalities for prostate cancer, effective anti-androgenic drugs which do not cause impotence must be developed. And the mechanism of androgen independence must be elucidated to obtain a more effective and complete hormonotherapy for prostate cancer.
authors.affiliation: Department of Urology, Kyoto University, School of Medicine, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Oishi
authors.forename: O
authors.initials: O
authors.lastname: Yoshida
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000726:Androgen Antagonists / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000139:chemically induced; D007172:Erectile Dysfunction / Q000139:chemically induced; D004967:Estrogens / Q000009:adverse effects / Q000627:therapeutic use; D007987:Gonadotropin-Releasing Hormone / Q000009:adverse effects / Q000627:therapeutic use; D006801:Humans; D008297:Male; D008875:Middle Aged; D009919:Orchiectomy; D011471:Prostatic Neoplasms / Q000188:drug therapy* / Q000601:surgery
chemical_list: D000726:Androgen Antagonists; D004967:Estrogens; D007987:Gonadotropin-Releasing Hormone