Abstract
Physiologic concentrations of estrogen stimulate precursor incorporation and growth in several lines of human breast cancer cells in long term tissue culture. Antiestrogens inhibit precursor incorporation and eventually kill the cells. Estrogens reverse antiestrogen effects. Responsive cell lines contain high affinity specific cytoplasmic receptors for estrogen. When binding and stimulation are measured under similar conditions, it appears that only a small proportion of receptor sites need be occupied for maximal stimulation. Thymidine kinase specific activity is increased by estradiol and may, in part, explain enhanced thymidine incorporation. These cell lines should prove useful for the study of the mechanisms by which estrogens regulate growth in human breast cancer
