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In this issue of the Journal, Song et al. (1) report that prolonged estrogen withdrawal in breast cancer cells results in the acquisition of an apoptotic response to 17 -estradiol; i.e., the very same hormone that mediates the proliferation of its target cells in the female genital tract and mammary glands is also able to trigger their death. In this editorial, we aim to integrate these experimental results, which are obviously relevant to the management of breast cancer, within a biologic perspective. The exploration of nature never ceases to surprise biologists. When adopting a narrow anthropocentric approach, we imagine nature as designed by a meticulous engineer. However, a more appropriate metaphor would be to imagine instead the workings of nature as the fruit of tinkering, or putting old devices to new uses. From this evolutionary perspective, it is conceivable that the same sex steroid hormones mediate the increase of cell numbers, the inhibition of cell proliferation, the inhibition of cell death, and the increase of cell death. In the 1970s, Bruchovsky et al. (2) showed that androgens, in addition to inhibiting cell death and inducing cell proliferation in the rat prostate in situ, inhibit prostate cell proliferation. The proliferative and inhibitory effects were dissociated temporarily; i.e., the latter event followed the former. Gorski and colleagues (3,4) described an equivalent effect by estrogens for the uterus and the pituitary gland.

The Two Faces of Janus: Sex Steroids as Mediators of Both Cell Proliferation and Cell Death