Summary This study aimed to investigate the effect of tamoxifen on breast tumour levels of oestrogen and progesterone receptor (ER and PR) and proliferation as defined by the Ki67 antibody. A group of primary breast cancer patients was randomised to receive either tamoxifen (n = 59) or placebo (n = 44) treatment in the interval between clinic and surgery (median 21 days). Frozen (McGuire & Clark, 1983 .Tumour proliferative activity is also related to the prognosis of breast cancer and a negative correlation has been observed between presence of ER and/or PR and the growth fraction as measured by a variety of methods. These methods include measurement of thymidine incorporation (Meyer et al., 1977;, estimation of the S phase fraction by DNA flow cytometry (Olszewski et al., 1981;Raber et al., 1982) and immunohistological staining using the mouse monoclonal antibody Ki67 (McGurrin et al., 1987) which recognises a proliferation-associated nuclear antigen present in the late Gl, S, G2 and M, but not in the Go, phases of the cell cycle (Gerdes et al., 1983;1984). As the endpoint of antioestrogen action is inhibition of tumour cell proliferation, a more functional approach to predicting response would be the measurement of proliferative activity before and during administration of a short course of tamoxifen.In the present study, we have used immunohistological methods to study breast tumour tissue before and after treatment with tamoxifen or a placebo in order to correlate and compare levels of expression of ER and PR with the proliferating cell-associated antigen defined by the monoclonal antibody Ki67, and with other histological data. The aim of the study was to elucidate the relationships between these factors before and after tamoxifen treatment in order to achieve a better prediction of response to endocrine treatment in individual patients.
Patients and methods
Patients