Acta Obstet Gynecol Scand 1992; 71 Suppl 155: 31-38 During the last two decades, considerable experimental evidence has been collected indicating that epithelial ovarian cancer might be gonadotropin dependent. LH and FSH receptors have been described in some of these tumors. The proliferation of ovarian cancer cells could be stimulated in vitro by gonadotropins. Suppression of endogenous LH and FSH secretion by GnRH-agonist treatment inhibited the growth of experimental or heterotransplanted ovarian cancers in various animal models. A number of recent phase II clinical trials have shown that the application of GnRH-agonists can lead to remission or stable disease in patients with relapsed advanced ovarian cancer. At present, prospective controlled clinical studies are being performed to assess the efficacy of GnRH-agonist treatment in addition to conventional surgical and cytostatic therapy in ovarian cancer in FIGO stages III and IV. Also, direct effects of GnRH analogues on ovarian cancer seem possible: a GnRH-like protein has been found in the human ovary. Our group discovered and partially characterized a specific GnRH-binding site (mol. wt 63.2 kDa) in ovarian cancer which is very similar to other human extrapituitary GnRHbinding sites of the low affinity, high capacity type, e.g. in breast cancer or the placenta. Recently, other groups have described also high affinity GnRH-agonist binding sites in ovarian cancer as well as in other extra pituitary tissues. First results from our laboratory indicate that the proliferation of certain ovarian cancer cell lines in vitro is reduced by both agonistic and antagonistic analogues of GnRH. Other authors were able to inhibit gonadotropin-induced in vitro proliferation of ovarian cancer cell lines by co-incubation with a GnRH-agonist. Thus GnRH -or a related compound -might act as an autocrine regulator of ovarian cancer proliferation, a finding which might be useful for the development of new therapeutic approaches.For more than a century it has been known that married women are much less likely to develop ovarian cancer (DC) than are unwed females (1). Some authors believed that this phenomenon was due to the suppression 'of the libido in unmarried women, causing hyperemia of the genital organs. Most gynecologists at that time, however, supposed that the higher incidence of DC in female celibates was caused by menstrual hyperemia, which occurred naturally more often in this population than in married women who had fewer menstruations due to pregnancies, child-bed and lactation (for review, see 2).Since the 1970s it has been shown by several investigators that the number of pregnancies and the duration of oral contraceptive use are significantly inversely related to the incidence of OC (e.g. 3-6). Fathalla (3) was the first to suggest that the incessant monthly ovulation which is characteristic of our species, in the 20th century at least, is a causal factor for the development of DC, due to the repeated rupture Acta Obstet Gynecol Scand Suppl J55