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82 Mehmet Topçul et al. Tamoxifen was first studied in the 1960s and emerged as a nonsteroidal antiestrogen for the treatment of breast cancer in the 1970s. Tamoxifen is now the prototypic hormonal agent used in breast cancer and its considerable success has prompted the investigation and development of newer antiestrogens. Tamoxifen possesses both antiestrogenic and estrogenic activity. Newer antiestrogens currently being developed may have fewer estrogens-agonistic properties and more potent antiestrogenic activity than tamoxifen. About one-third of breast cancer patients with advanced disease respond to treatment with the antiestrogen tamoxifen (Mc Guire et al., 1978) and most of them are patients with an estrogen positive primary tumour (Mouridsen et al., 1992; Rose et al., 1980). Epirubicin (Farmorubicin) is a new derivative of doxorubicin, synthesized with the aim of finding anthracycline analogues with an improved spectrum of antitumour activity and lower toxicity. It appears to have similar antitumour activity and toxicity as the parent drug in experimental and human tumours. Epirubicin has been used alone or in combination with other cytotoxic agents. In vitro cell culture studies show that epirubicin enters the cell nuclei, inhibits nucleic acid synthesis and arrests cell division (Di Marco, 1984; Skladannowski and Konopa, 1994). In the present study, we investigated the effect of epirubicin and tamoxifen on labelling index of FM3A cells in other to increase chance of this drugs in clinical applications. Material and methods Cells We used estrogen receptor (ER) positive FM3A cell line in our experiments. C3H mouse mammary carsinoma-derived FM3A cell line grown in RPMI 1640+10% Fetal Bovine Serum as suspension culture have been used in tissue culture studies in recent years. Test cells were divided into one control and three test groups. Microplate wells were covered with 10 4 cells/ml and incubated 5% CO2 and 95% air for 24 hours. Estrogen receptor assay ER levels were studied by the methods of Lippman and Huff (1976) and Raynaud et al. (1978) with minor modifications. ER activity as demonstrated by the dextran-coated charcoal tecnique is closely correlated with the clinical ability of tamoxifen to inhibit tumour growth. Drug application We used optimum doses of epirubicin and tamoxifen. At first, we investigated optimum doses for FM3A cells. These doses were found 0.01 mg/ml for epirubicin and 0.001 mg/ml for tamoxifen. At the end of the 24 hour incubation, the medium was replaced with a medium containing epirubicin, tamoxifen and epirubicin+tamoxifen doses and reincubated 0, 4, 8, 16 and 32 hours. Labelling index For labelling index determination, cells were then incubated with RPMI 1640 containing 5 µCi/ml 3 H-TdR(Amersham). Both control and treated cells were labelled for 1 hour. Smeared cells were than prepared on glass-slides. Slides were rinsed with 2% perchloric acid twice at 4°C for 30 minutes to remove dissolved radioactive material. They were then coated with K2 emulsion (Ilford), kept at 4°C for 3 days, and developed. Labelling index was calculated by counting at least the 3000 cells from each slide, stained with Giemsa for 3 minutes. Statistical analysis Student-t test was used to evalute the results (n=150). Results Figure 1 indicates labelling index values of Control, 0.01 mg/ml epirubicin, 0.001 mg/ml tamoxifen and 0.01 mg/ml epirubicin + 0.001 mg/ml tamoxifen groups after an application of 0, 4, 8, 16 and 32 hours. After 4 hours treatment, when various concentrations of epirubicin, tamoxifen and
epirubicin + tamoxifen were added to the cultures, DNA synthesis decreases minimum with respect to the control cells (p
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