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The cause of cancer of the ovaries is unclear, but receptors for certain hormones on the surfaces of cancer cells have been implicated. The cell receptors are thought to have a particular affinity for follicle stimulating hormone (FSH), luteinizing hormone (LH) or human chorionic gonadotropin (HcG), although involvement of this latter hormone is controversial. Tumor specimens from 29 patients with ovarian cancer were evaluated for hormone binding sites. Sites for FSH were found on five tumor samples. Sites for LH were found on two tumor samples. These binding sites were found in the stromal layer of the ovarian tissue. The way these hormone receptor sites respond to gonadotropin hormones needs to be investigated.

The binding of human LH and human FSH to postmenopausal ovarian tissue from 21 patients with cervical carcinoma was analyzed. The binding sites for FSH and LH were demonstrated in postmenopausal ovarian tissue. The surface-binding autoradiographic study revealed that the binding sites for gonadotropins were localized in the cells of cortical stroma of the postmenopausal ovary. In addition, diffuse cytoplasmic staining of endogenous estrogen and 3β−hydroxysteroid dehydrogenase activity were detected immunohistochemically and histochemically in the cells of the cortical stroma. Electron microscopic study also suggested steroidogenic function in the cells of the cortical stroma. The results of the present study suggest that postmenopausal ovaries contain specific binding sites for pituitary gonadotropins and play a role in ovarian steroidogenesis. (Obstet Gynecol 73196, 1989)

Epidermal growth factor (EGF) modulates ovarian function, including folliculogenesis and steroidogenesis. We investigated the localization of EGF binding sites in the porcine ovary, and the effect of FSH on EGF binding to cultured granulosa cells. Autoradiographic study demonstrated that the binding sites for 125I-labeled mouse EGF in the porcine ovary were present in the granulosa and luteal cells, but not in the thecal cells. Porcine granulosa cells were collected by the needle aspiration method from small (1–2 mm) and medium-sized (3–5 mm) follicles. Scatchard analysis showed that a single class of the specific binding sites for EGF was present in the granulosa cells. The number of binding sites and the apparent dissociation constant were 5 540 binding sites/cell and 0.23 nM (medium-sized follicle), respectively. No significant difference was observed between small and medium-sized follicles. Granulosa cells were cultured for 48 h at 37°C in medium alone or with increasing doses of ovine FSH (1–100 ng/ml). FSH treatment significantly increased EGF binding in a dose-dependent manner.In conclusion, it is suggested that the specific high affinity, low capacity binding sites for EGF are present in porcine granulosa cells, and that they are up-regulated by FSH.

Immunohistochemical localization of pituitary gonadotropins (FSH, LH) and estrogen was investigated in 17 ovaries from ten postmenopausal women. Positive immunostaining for 17β-estradiol was demonstrated in the cortical stroma of 14 postmenopausal ovaries. Positive immunostaining for FSH was localized in the cortical stroma of 12 postmenopausal ovaries, and positive immunostaining for LH was also localized in 12 ovaries. Immunohistochemical localization for pituitary gonadotropins (FSH and/ or LH) and 17β-estradiol was identified in the same hypertrophic cortical stroma of 13 postmenopausal ovaries. The ultrastructural study suggested steroidogenic activity in the cortical stromal cells of the postmenopausal ovary. In addition, peripheral and ovarian venous concentrations of 17β-estradiol were measured in 13 postmenopausal subjects, and significant concentration gradient for serum 17β-estradiol was noted. The ovarian/peripheral concentration gradient for 17β-estradiol had a tendency to be higher in the subjects with positive immunostaining for 17β-estradiol compared with that in the subjects with negative immunostaining. The present results suggest that the human ovary secretes estrogen in response to pituitary gonadotropins even after the menopause.