Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Effect of a gonadotropin releasing hormone analog on an experimental ovarian tumor: direct and indirect actions. 759 32

An ovary implanted into the spleen of an ovariectomized rat develops into a luteinized tumor, growing in response to gonadotrophins. Previously, it was shown that in vivo Buserelin, a gonadotrophin-releasing hormone (GnRH) analog, inhibited tumor growth. To determine if GnRH had a direct effect on tumor cells, the presence of GnRH receptors as well as the endocrine effects of buserelin were studied on tumoral tissue. GnRH receptors were present in luteoma in similar concentrations and dissociation constant (Kd) to control estrous ovaries. In vivo treatment with buserelin did not modify luteoma GnRH receptors. In organ incubations, luteoma secreted significantly higher estradiol and lower progesterone than estrous ovaries; addition of buserelin did not modify steroid secretion. The same difference in basal steroid secretion between luteoma cells and luteal cells superovulated prepubertal ovaries was observed in cell cultures. Although luteinizing-hormone (LH)-stimulated progesterone in both kinds of cells, buserelin significantly inhibited LH-stimulated progesterone only in luteoma cells. These results describe clear differences in basal steroid secretion between tumoral and normal tissue. Furthermore, they show that luteoma possess GnRH receptors similar to those in normal ovarian tissue, and that GnRH analogs have endocrine effects on these cells. Therefore, a direct effect of buserelin on luteoma cells can be postulated.
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PMID:GnRH receptors and GnRH endocrine effects on luteoma cells. 922 31