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Induction of mammary gland ductal hyperplasias and carcinoma in situ following fetal bisphenol A exposure.


ABSTRACT: Exposure of the fetus to excess estrogen is believed to increase the risk of developing breast cancer during adult life. Fetal exposure to low doses of the xenoestrogen bisphenol A resulted in long-lasting effects in the mouse mammary gland that were manifested during adult life. It enhanced sensitivity to estradiol, decreased apoptosis, increased the number of progesterone receptor-positive epithelial cells at puberty and increased lateral branching at 4 months of age. We now report that fetal exposure to 2.5, 25, 250 and 1000 microg bisphenol A/kg body weight/day induces the development of ductal hyperplasias and carcinoma in situ at postnatal day 50 and 95 in rats. These highly proliferative lesions have an increased number of estrogen receptor-alpha positive cells. Thus, fetal bisphenol A exposure is sufficient to induce the development of preneoplastic and neoplastic lesions in the mammary gland in the absence of any additional treatment aimed at increasing tumor development.

SUBMITTER: Murray TJ 

PROVIDER: S-EPMC1987322 | biostudies-literature | 2007 Apr-May

REPOSITORIES: biostudies-literature

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Induction of mammary gland ductal hyperplasias and carcinoma in situ following fetal bisphenol A exposure.

Murray Tessa J TJ   Maffini Maricel V MV   Ucci Angelo A AA   Sonnenschein Carlos C   Soto Ana M AM  

Reproductive toxicology (Elmsford, N.Y.) 20061024 3


Exposure of the fetus to excess estrogen is believed to increase the risk of developing breast cancer during adult life. Fetal exposure to low doses of the xenoestrogen bisphenol A resulted in long-lasting effects in the mouse mammary gland that were manifested during adult life. It enhanced sensitivity to estradiol, decreased apoptosis, increased the number of progesterone receptor-positive epithelial cells at puberty and increased lateral branching at 4 months of age. We now report that fetal  ...[more]

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