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Journal of Clinical Endocrinology & Metabolism, Vol 59, 441-446, Copyright © 1984 by Endocrine Society
ARTICLES |
RL Stouffer, MS Grodin, JR Davis and EA Surwit
The binding of FSH and hCG to ovarian tumor biopsies from 31 women was analyzed to determine whether ovarian cancers contain receptors for gonadotropic hormones. For comparative purposes, gonadotropin binding to receptor-positive control tissues was also assessed. Specific binding was defined as [125I]hFSH and [125I]hCG binding prevented by coincubation of tissue samples with an excess of unlabeled gonadotropin. Various types of epithelium-derived tumors (serous, mucinous, endometrioid, and undifferentiated; n = 29) had low levels of specific FSH and hCG binding (less than 15% of receptor-positive control tissues) which were not dependent on tissue concentration and not saturable. A germ cell tumor had similar binding characteristics. In contrast, specific FSH binding to a granulosa cell-theca cell (GC- TC) tumor was directly proportional to tissue concentration, and binding was maximal in the presence of 100 ng/ml [125I]FSH. Scatchard analyses of FSH binding yielded a linear plot. Although the FSH-binding capacity of the GC-TC tumor (6.3 fmol/mg) exceeded that of control tissues, their binding affinities (Kd = 1.4 X 10(-9)M) were similar. Specific hCG binding to the GC-TC tumor was low and not dependent on tissue concentration. We conclude that the specific binding of FSH to the GC-TC tumor was characteristic of the interaction of gonadotropin with receptors in target tissues. However, the low level of FSH and hCG binding to tumors of epithelial origin did not represent gonadotropin- receptor binding. Thus, the common ovarian tumors of epithelial origin may not respond directly to gonadotropin, but malignancies of sex cord- stromal origin, such as GC-TC tumors, could be modulated by FSH.
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