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Androgens and Mammary Ca Fer Ster 02 FERTILITY AND STERILITY௡ VOL. 77, NO. 4, SUPPL 4, APRIL 2002 ANDROGEN EFFECTS ON Copyright ©2002 American Society for Reproductive Medicine Published by Elsevier Science Inc. FEMALE HEALTH Printed on acid-free paper in U.S.A. Androgens and mammary growth and neoplasia Constantine Dimitrakakis, M.D., Jian Zhou, M.D., and Carolyn A. Bondy, M.D. Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland Objective: Evaluation of current clinical, experimental, genetic, and epidemiological data pertaining to the role of androgens in mammary growth and neoplasia. Design: Literature review. Setting: National Institutes of Health. Subject(s): Recent, basic, clinical, and epidemiological studies. Intervention(s): None. Main Outcome Measure(s): Effects of androgens on mammary epithelial proliferation and/or breast cancer incidence. Result(s): Experimental data derived from rodents and cell lines provide conflicting results that appear be strain- and cell line–dependent. Epidemiologic studies have significant methodological limitations and provide inconclusive results. The study of molecular defects involving androgenic pathways in breast cancer is in its infancy. Clinical and nonhuman primate studies, however, suggest that androgens inhibit mammary epithelial proliferation and breast growth and that conventional estrogen treatment suppresses endogenous androgens. Conclusion(s): Abundant clinical evidence suggests that androgens normally inhibit mammary epithelial proliferation and breast growth. Suppression of androgens by conventional estrogen treatment may thus enhance estrogenic breast stimulation and possibly breast cancer risk. Clinical trials to evaluate the impact of combined estrogen and androgen hormone replacement regimens on mammary gland homeostasis are needed to address this issue. (Fertil Steril௡ 2002;77(Suppl 4):S26–33. ©2002 by American Society for Reproductive Medicine.) Key Words: Breast cancer, estrogen, androgen receptor, testosterone, oral contraceptive, hormone replace- ment The importance of estrogens in stimulating genic stimulation of mammary epithelial mammary epithelial proliferation and breast proliferation and hence potentially breast can- growth and in increasing the risk for breast cer risk. This is because the suppression of Received October 16, cancer is well established. The normal ovary gonadotropins by exogenous E treatment re- 2001; revised and produces relatively larger amounts of androgen sults in globally reduced ovarian steroidogen- accepted January 9, 2002. compared with estrogens (Es), however, and a esis, so both endogenous E and androgen pro- Reprint requests: Carolyn variety of clinical and experimental observa- duction are reduced, but only Es are provided A. Bondy, M.D., Developmental tions suggest that androgens normally inhibit by the treatment regimens. Moreover, Es, par- Endocrinology Branch, estrogenic effects on mammary growth. Both ticularly in oral form, stimulate the hepatic National Institute of Child androgen and E receptors are expressed in production of sex hormone–binding globulin Health and Human Development, National mammary epithelium (1, 2), suggesting that the (SHBG), which binds testosterone (T) with Institutes of Health, steroid hormone effects may be integrated at high affinity, reducing androgen bioavailabil- Building 10, Room 10N262, the level of the mammary epithelial cell. ity. As a result of these dual effects, both total 10 Center Drive, MSC and bioavailable T levels are significantly re- 1862, Bethesda, Maryland Recent experimental data suggest that con- 20892-1862 (FAX: duced in women taking OCs or E replacement ventional E treatment regimens, both as oral 301-402-0574; E-mail: for ovarian insufficiency (4). [email protected]). contraceptives (OCs) (3) and as hormone “re- placement therapy” (1), upset the normal E–an- This review of the literature was prompted 0015-0282/02/$22.00 PII S0015-0282(02)02979-5 drogen balance and promote unopposed estro- by our concern that the iatrogenic reduction in S26 androgens in women on E therapy might contribute to un- opposed estrogenic stimulation of the breast and potentially FIGURE 1 augment breast cancer risk. Schematic design of the androgen receptor gene (top) and protein (below). The polymorphic trinucleotide repeat site is indicated at the left. Transactivating function (TAF), DNA- ESTROGENS, ANDROGENS, AND binding (DBD), and ligand-binding domains (LBD) are la- BREAST DEVELOPMENT beled. Estrogens stimulate and androgens inhibit breast devel- opment, independent of genetic sex. Pubertal rises in E levels cause breast growth in girls (5) and frequently in boys (transiently) (6). Estradiol levels are significantly higher in girls with premature thelarche than in normal prepubertal girls (7). Recently, an association between expression of a high-activity isoform of the T-metabolizing CYP3A4 and the early onset of thelarche has been documented, suggesting that decreasing T levels may also trigger early breast growth Dimitrakakis. Androgens and the mammary gland. Fertil Steril 2002. (8). Conversely, androgen excess caused by adrenal tumor or hyperplasia suppresses normal breast development in girls, despite apparently adequate E levels (9–11). In castrated of androgen effectors in women are derived from such an male-to-female transsexuals, feminizing E therapy stimu- intracrine mode of action, which will not be detected by lates breast growth with full acinar and lobular formation assays of circulating T or dihydrotestosterone (DHT). Inter- (12), and E-treated genetically male breast tissue exhibits estingly, whereas circulating levels of T and DHT are 5- to normal female histology. Estrogens taken to treat prostate 10-fold higher in men than in women, the abundance of cancer also lead to breast development in men with sup- androgen metabolites is less than twofold higher in men, pressed gonadal function and reduced T levels (13). Con- suggesting that local tissue production and action of andro- versely, androgen use by female athletes and female-to-male gens in women may be more significant than previously transsexuals leads to breast atrophy (14, 15). suspected. Supporting the normal inhibitory role of endogenous an- Pertinent to this review, the mammary gland is capable of drogens on breast growth, androgen receptor (AR) blockade the synthesis of both E2 and T. All the steroidogenic en- with flutamide causes gynecomastia (16), and AR deletion or zymes necessary for the formation of androgens and Es from inactivating mutation is associated with macromastia (and steroid precursors—namely steroid sulfatase, 17␤-hydroxys- increased breast cancer). Males may also develop gynecom- teroid dehydrogenases, 3␤-hydroxysteroid dehydrogenases, astia when the E–androgen ratio is increased because of 5␣-reductases, and aromatase—have been reported in nor- decreased androgen production or increased aromatization mal mammary tissues, breast cancer specimens, or cell lines (6). (21–24). Breast cancer cell lines and tissue specimens ex- It has not been possible to identify specificE–androgen press the enzymes involved in DHT as well as in E2 synthe- ratios predictive of breast stimulation or inhibiting effects for sis (21, 25–27). In a recent histochemical study, expression ␣ several reasons. Estradiol and T assays have traditionally not of 5 -reductase was significantly correlated with AR expres- ␤ been very sensitive in the lower ranges, and both hormones sion and 17 -hydroxysteroid dehydrogenase (HSD) (5) and ␤ bind to SHBG, so total values may not be as informative as 3 -HSD immunoreactivities, and the abundance of this an- values of free or bioavailable hormone (4). Moreover, sin- drogenic molecular assembly was inversely correlated with gle-hormone measurements may not be very informative tumor size, histological grade, and proliferative index (21), suggesting an inhibitory role for DHT in tumor growth. about tissue exposure over time. Both E2 and T levels vary from hour to hour in response to diurnal rhythms, diet, stress, and exercise (17, 18), so a single value may be inadequate to ANDROGEN RECEPTOR assess true tissue exposure. Androgen agonists such as T and DHT function by bind- In addition, E2 and T may be synthesized locally in ing to the intracellular AR, which is a member of the nuclear peripheral tissues from circulating precursors such as DHEA hormone receptor superfamily comprising classic DNA- or DHEAS and androstenedione (reviewed in references 19, binding, hormone-binding, and activation domains (Fig. 1). 20). The conjugated products of steroid metabolism find Androgen receptor expression is abundant in normal mam- their way into the circulation after peripheral action and mary epithelium and in the majority of breast cancer speci- provide evidence as to the proportion of the precursor pools mens and cell lines (1, 2, 28, 29). The AR is colocalized with of steroids used as androgen or E. Analyses of these metab- E and progesterone receptors in epithelial cells but is not olites by Labrie et al. (20) suggest that the major proportion detected in mammary stroma or myoepithelium (1, 30, 31). FERTILITY & STERILITY௡ S27 The coexpression of ER and AR in mammary epithelial cells Attempts to correlate adrenal precursor steroids with suggests that the effects of E and androgen on mammary breast cancer incidence have been relatively more successful epithelial proliferation are integrated within the mammary or at least consistent, perhaps reflecting
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