Effect of a gonadotropin releasing hormone analog on an experimental ovarian tumor: direct and indirect actions

• Published in: Life sciences (1973) Vol. 57; no. 3; p. 291
• Main Authors: Lux-Lantos, V A, Thyssen, S M, Chamson, A, Libertun, C
• Format: Journal Article
• Language: English
• Published: Netherlands 1995
• Subjects: Animals; Estradiol - blood; Female; Follicle Stimulating Hormone - blood; Gonadotropin-Releasing Hormone - analogs & derivatives; Gonadotropin-Releasing Hormone - pharmacology; Luteinizing Hormone - blood; Luteoma - drug therapy; Luteoma - pathology; Ovarian Neoplasms - drug therapy; Ovarian Neoplasms - metabolism; Ovarian Neoplasms - pathology; Progesterone - metabolism; Rats; Rats, Sprague-Dawley; Tumor Cells, Cultured
• ISSN: 0024-3205
• DOI: 10.1016/0024-3205(95)00272-8

An ovary autotransplanted into the spleen of a bilaterally ovariectomized rat develops into a luteoma, which grows under constant gonadotropin hyperstimulation. The effect of a long-acting GnRH agonist (GnRH-a), on tumor growth and hormone secretion was investigated. Two experimental models were used: Model 1: GnRH-a (0.33 mg/rat sc) or estradiol valerianate (50 micrograms/rat sc injected once a week for four weeks) was administered simultaneously with ovary implantation; Model 2: the drugs were administered after 1 month of tumor development. The treatment with estradiol was used as a control of tumor regression. Saline injected ovarian grafted rats and Sham operated animals were used as controls. In Model 1: The GnRH-a significantly inhibited tumor development (Positive tumors: Saline: 100% vs GnRH-a: 43%, p < 0.01). In Model 2: the GnRH-a and estradiol significantly reduced the volume of one month old tumors (52% and 39% of initial volumes respectively, p < 0.01). Gonadotropin secretion was significantly inhibited or its increase blunted by the GnRH-a and by estradiol treatments in both models. Estradiol and progesterone in portal blood, which collects the steroids secreted by the luteoma, were significantly reduced by GnRH-a treatment in both models. On the other hand, in tumor cells cultured "in vitro", the GnRH-a was able to inhibit the LH induced progesterone secretion in a concentration dependent way. These results clearly show that the GnRH-a is effective in inhibiting tumor growth or reducing its volume, when already developed; furthermore, it suppresses tumor steroid hormone production. These actions were exerted at both the hypophyseal and tumor levels.