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Objective

The normal ovary produces abundant testosterone in addition to estradiol (E 2) and progesterone, but usually only the latter two hormones are “replaced” in the treatment of ovarian failure and menopause. Some clinical and genetic evidence suggests, however, that endogenous androgens normally inhibit estrogen-induced mammary epithelial proliferation (MEP) and thereby may protect against breast cancer.

Design

To investigate the role of endogenous androgen in regulating mammary epithelial proliferation, normal-cycling rhesus monkeys were treated with flutamide, an androgen receptor antagonist. To evaluate the effect of physiological testosterone (T) supplementation of estrogen replacement therapy, ovariectomized monkeys were treated with E 2, E 2 plus progesterone, E 2 plus T, or vehicle.

Results

We show that androgen receptor blockade in normal female monkeys results in a more than …