No abstract

Bei insgesamt 197 malignen Ovarialtumoren wurden Östrogenrezeptoren (ER) und Progesteronrezeptoren (PR) bestimmt. In epithelialen Ovarialkarzinomen war die Häufigkeit der Rezeptoren wie in Mammakarzinomen (ER in 64%, PR in 49% der Fälle). Bei den nicht epithelialen Tumoren wurden Steroidrezeptoren nur in Granulosazell-tumoren gefunden. Die Häufigkeit von Progesteronrezeptoren nahm ab bei Metastasierung und bei Vorbehandlung mit einer Chemotherapie. Ebenso hatten Ovarialkarzinome in der Postmenopause seltener Progesteronrezeptoren als prämenopausal (52% bzw. 71%), Östrogenrezeptoren waren jeweils unverändert. Tumoren, die auf eine zytostatische Chemotherapie mit einer Remission reagierten, waren häufiger PR-negativ als Tumoren mit Progression oder no-change-Verhalten. Möglicherweise ist die Überlebenswahrscheinlichkeit bei PR-negativen Ovarialkarzinomen größer als bei PR-positiven. Eine Abhängigkeit zwischen klinischem Tumorstadium oder histologischem Grade und Steroidrezeptoren bestand nicht.

Estrogen receptors (ER) and progesterone receptors (PR) were evaluated in 173 primary ovarian cancers and in 6 ovarian metastases. In epithelial ovarian carcinomas 63% had ER and 46% PR. Almost all granulosa cell tumours were receptor-positive, while sarcomas, dysgerminomas, and teratomas lacked ER and PR. Both receptors were found less often in tumours of the histological grade I than in those of grade II and III. During the development of metastases and during chemotherapy there was a loss of PR in 27% and 53% of the cases, respectively, while the amount of ER remained more or less constant. In addition to ovarian cancers ER and PR were present in carcinomas of the fallopian tube as well. ER-negative and especially PR-negative tumours seemed to respond better to chemotherapy than receptor-positive carcinomas. The possible significance of ER and PR with regard to the success of an endocrine treatment is discussed.

As previously reported, ovarian epithelial carcinomas may respond to endocrine therapy. We examined the direct effect of progesterone, medroxyprogesteroneacetate, gestoneron, 17-beta-estradiol, tamoxifen, 4-OH-tamoxifen, or N-desmethyltamoxifen on the proliferative capacity of ovarian carcinoma cells by means of the colony assay described by Hamburger and Salmon. The growth rate of 25 tested tumors (ascitic fluid, primary tumor, metastases) was 68%. The plating efficiency was 0.078%. Beside the drug testing estrogen and progesterone receptor levels were determined. The inhibition of colony survival was slightest with 17-beta-estradiol, more pronounced with medroxyprogesteroneacetate, gestoneron, N-desmethyltamoxifen, and progesterone, and greatest with 4-OH-tamoxifen and tamoxifen. Significant and dose-dependent inhibition of greater than 70% was observed with tamoxifen and 4-OH-tamoxifen in 80% of the tested tumors. There was no significant correlation between the in vitro responsiveness and the level of hormonal act not only via an estrogen receptor but also via an antiestrogen-binding site.

No abstract