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In vitro responsiveness of ovarian epithelial carcinomas to endocrine therapy
Abstract:
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.
Insights
Tamoxifen and its metabolite 4-OH-tamoxifen show significant efficacy in inhibiting ovarian carcinoma cell proliferation. These findings suggest potential for endocrine therapy in treating ovarian epithelial carcinomas.
Area of Science:
- Oncology
- Endocrinology
- Cell Biology
Background:
- Ovarian epithelial carcinomas are a significant cause of cancer-related mortality in women.
- Previous research indicates that some ovarian carcinomas may respond to endocrine therapy, highlighting the potential role of hormone-based treatments.
Purpose of the Study:
- To investigate the direct impact of various endocrine agents on the proliferative capacity of ovarian carcinoma cells.
- To evaluate the efficacy of specific hormones and antiestrogens in inhibiting tumor cell growth in vitro.
Main Methods:
- Utilized the colony assay (Hamburger and Salmon) to assess the proliferative capacity of ovarian carcinoma cells from 25 tumors.
- Determined estrogen and progesterone receptor levels alongside drug testing.
- Administered progesterone, medroxyprogesterone acetate, gestoneron, 17-beta-estradiol, tamoxifen, 4-OH-tamoxifen, and N-desmethyltamoxifen to cell cultures.
Main Results:
- Tamoxifen and 4-OH-tamoxifen demonstrated the greatest inhibition of colony survival, achieving >70% inhibition in 80% of tested tumors.
- Medroxyprogesterone acetate, gestoneron, N-desmethyltamoxifen, and progesterone showed moderate inhibition.
- 17-beta-estradiol exhibited the least inhibitory effect.
- No significant correlation was found between in vitro responsiveness and hormone receptor levels.
Conclusions:
- Tamoxifen and 4-OH-tamoxifen are potent inhibitors of ovarian carcinoma cell proliferation in vitro.
- The antiestrogen tamoxifen and its active metabolite 4-OH-tamoxifen show promise for endocrine therapy in ovarian cancer.
- Ovarian carcinoma cell growth may be modulated via estrogen receptors and antiestrogen-binding sites.