Constantine Dimitrakakis1, Jian Zhou, Carolyn A Bondy. 1. Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.
Abstract
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.
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.
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