Hormonal profiles in women with breast cancer (review)

Abstract

The literature concerning endogenous hormonal profiles in women with breast cancer and breast-cancer risk has been critically reviewed. The many published reports have been divided into 11 groups, with each group centered on a particular hypothesis that has been either explicitly formulated by the authors of the reports or perceived by other workers as a unifying hypothesis in certain studies. The hypotheses reviewed are: the adrenal androgen insufficiency hypothesis, the anovulation/luteal inadequacy hypothesis, the estriol hypothesis, the ovarian androgen excess hypothesis, the thyroid dysfunction hypothesis, the prolactin hypothesis, the estrone hypothesis, the estrogen-window hypothesis, the estrogen-excess hypothesis, the melatonin hypothesis, and the estrogen hydroxylation hypothesis. It is concluded that there remain, at present, only four viable hypotheses: the hypotheses of increased risk with adrenal androgen deficiency, ovarian dysfunction (luteal inadequacy and excessive ovarian androgen secretion), increased 16 alpha-hydroxylation of estradiol, and the hypothesis of decreased risk with pregnancy-induced lowering of prolactin levels. Adrenal androgen deficiency seems to be pertinent only in premenopausal cancer patients, and may be a genetic defect. Ovarian dysfunction seems to be pertinent to both premenopausal and post-menopausal patients and may also have a strong genetic component. Increased estradiol hydroxylation likewise seems to have a genetic component. The prolactin effect differs from the others, in that it is clearly environmental, rather than genetic, and may represent a permissive effect rather than a true risk-promoting effect.