A long-acting gonadotropin-releasing hormone agonist inhibits the growth of a human ovarian epithelial carcinoma (BG-1) heterotransplanted in the nude mouse

Human ovarian epithelial carcinoma (BG-1) was heterotransplanted in female nude athymic mice and growth was evaluated in intact, surgically castrated, and gonadotropin-releasing hormone (GnRH) agonist (Lupron-SR)-treated mice. Tumor volume was represented as percent of tumor volume on day 0 and measured every other day from the administration of drug and/or the attainment of a minimum tumor volume of 0.5 cm3 on each side of the animal. Tumors in surgically castrated mice had significantly accelerated growth compared with control tumors grown in intact mice (1810 +/- 247.2 versus 1253.6 +/- 44.6%, respectively; P less than .05). Treatment with GnRH agonist significantly reduced tumor growth in intact mice at days 16, 18, and 20 compared with normal control tumors and placebo-treated tumors in intact mice (P less than .02). Gonadotropin levels in pooled serum of mice were reduced from normal levels with GnRH agonist treatment (control: mLH 16.9 +/- 2.2 ng/mL, mFSH 6.6 +/- 0.3 ng/mL; GnRH agonist-treated: mLH 9.3 +/- 1.8 ng/mL, mFSH 4.9 +/- 0.7 ng/mL; surgically castrated: mLH 32.2 +/- 2.7 ng/mL, mFSH 19.4 +/- 0.5 ng/mL). This human tumor model appears responsive to gonadotropins as evidenced by the ability of a GnRH agonist to inhibit growth of BG-1. These results suggest that GnRH agonist therapy may be a useful adjuvant in the treatment of human ovarian epithelial carcinoma.