Abstract

Estradiol induces proliferation of ZR-75.1 human breast cancer cells cultured as a monolayer using minimum essential medium supplemented with 10% charcoal treated fetal bovine serum. Comparing continuous and pulsatile estradiol treatment we could not observe any amplification or limitation of growth effects when we corrected for the different time of exposure. We could perfectly predict cell number by summarizing growth effects of all estradiol pulses and therefore conclude that estrogen receptor is a “sensor” that measures the time of estradiol exposure in a linear manner whereas the estradiol concentration is recognized in a non-linear fashion as predicted by the law of mass action which governs steroid-receptor interaction.

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