title: Estrogens in the wrong place at the wrong time: Fetal BPA exposure and mammary cancer.
abstract: Iatrogenic gestational exposure to diethylstilbestrol (DES) induced alterations of the genital tract and predisposed individuals to develop clear cell carcinoma of the vagina as well as breast cancer later in life. Gestational exposure of rodents to a related compound, the xenoestrogen bisphenol-A (BPA) increases the propensity to develop mammary cancer during adulthood, long after cessation of exposure. Exposure to BPA during gestation induces morphological alterations in both the stroma and the epithelium of the fetal mammary gland at 18 days of age. We postulate that the primary target of BPA is the fetal stroma, the only mammary tissue expressing estrogen receptors during fetal life. BPA would then alter the reciprocal stroma-epithelial interactions that mediate mammogenesis. In addition to this direct effect on the mammary gland, BPA is postulated to affect the hypothalamus and thus in turn affect the regulation of mammotropic hormones at puberty and beyond.
authors.affiliation: Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, United States. Electronic address: Tessie.Paulose@tufts.edu.
authors.forename: Tessie
authors.initials: T
authors.lastname: Paulose
authors.affiliation: Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, United States. Electronic address: Lucia.Speroni@tufts.edu.
authors.forename: Lucia
authors.initials: L
authors.lastname: Speroni
authors.affiliation: Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, United States. Electronic address: Carlos.Sonnenschein@tufts.edu.
authors.forename: Carlos
authors.initials: C
authors.lastname: Sonnenschein
authors.affiliation: Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, United States. Electronic address: Ana.Soto@tufts.edu.
authors.forename: Ana M
authors.initials: AM
authors.lastname: Soto
mesh_terms: D000367:Age Factors; D000818:Animals; D001559:Benzhydryl Compounds / Q000633:toxicity*; D001943:Breast Neoplasms / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D002450:Cell Communication / Q000187:drug effects; D002471:Cell Transformation, Neoplastic / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D004305:Dose-Response Relationship, Drug; D052244:Endocrine Disruptors / Q000633:toxicity*; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D004967:Estrogens / Q000633:toxicity*; D005260:Female; D005865:Gestational Age; D006801:Humans; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism; D008321:Mammary Glands, Animal / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism / Q000473:pathology; D042361:Mammary Glands, Human / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism / Q000473:pathology; D018811:Maternal Exposure / Q000009:adverse effects*; D010636:Phenols / Q000633:toxicity*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D018570:Risk Assessment; D012307:Risk Factors; D017154:Stromal Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D052244:Endocrine Disruptors; D004967:Estrogens; D010636:Phenols; C006780:bisphenol A; D000098826:Bisphenol A Compounds
keywords: Endocrine disruptors; Environmental exposure; Fetal mammary gland; Mammary gland development; Prenatal exposure; Xenoestrogens