LIMITED EFFECTS OF ANTIANDROGENS AND GONADOTROPIN-RELEASING HORMONE AGONIST ON TRANSPLANTABLE HUMAN PROSTATIC CANCER HONDA

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Human prostatic cancer transplanted into nude mice (HONDA) was treated with nonsteroidal antiandrogen, flutamide (FLT) or steroidal antiandrogen, chlormadinone acetate (CMA), with the doses of 50 mg and 200 mg for 28 days, and with a 5 μg daily dose of gonadotropin-releasing hormone agonist, leuprolide (LEU), for 8 weeks separately. Administration of 200 mg of FLT showed the most significant inhibition of the tumor growth followed in decreasing order by 200 mg of FLT, and 50 mg FLT. Monotherapy with 50 mg of CMA showed no effect on the growth of the tumor, suggesting that FLT is more potent antiandrogen than CMA. However, there was no reduction of the tumor weight despite the treatment with these agents. Orchiectomy markedly reduced the tumor weight. The weight of seminal vesicles and ventral prostate of the host mice were reduced significantly after the treatment with these antiandrogens, suggesting that there was substantial suppression of endogenous androgen action in these organs. Notable reduction of serum human prostatic acid phosphatase in the tumor-bearing mice was observed. Monotreatment with LEU did not inhibit the tumor growth, indicating the impairment of pituitary-gonadal axis of the nude mice. There was no changes in the content of the androgen receptor in the tumor cells regardless of the treatment. These results indicate that inhibitory effects of the antiandrogens in this experimental system is by direct cellular action. Although orchiectomy indicates the total androgen blockade in the mice, the discrepancy between the continuous tendency of the tumor growth notwithstanding antiandrogen treatment and the suppression of the endogenous androgen action suggests that growth-promoting factors other than androgens exist in the cancer family.
群馬大学の論文
1995-03-31

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