Abstract
A conditional tetracycline-responsive transgenic mouse model with deregulated estrogen receptor alpha expression in mammary epithelial cells developed ductal hyperplasia (DH), lobular hyperplasia, and ductal carcinoma in situ (DCIS) by 4 months of age. Higher proliferative rates were found in both normal and abnormal ductal and lobular structures. DH and DCIS but not normal ductal structures showed an increased percentage of cells with nuclear-localized cyclin D1. No differences in either the prevalence or extent of these phenotypes following exogenous 17beta-estradiol treatment were found suggesting that alteration of ERalpha expression was the rate-limiting factor in initiation of DH, lobular hyperplasia, and DCIS.
Publication types
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Carcinoma in Situ / genetics
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Carcinoma in Situ / metabolism*
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Carcinoma, Ductal / genetics
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Carcinoma, Ductal / metabolism*
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Cell Nucleus / metabolism
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Cell Proliferation
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Cell Transformation, Neoplastic / genetics
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Cell Transformation, Neoplastic / metabolism
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Cyclin D1 / metabolism
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Estradiol / pharmacology
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Estrogen Receptor alpha / biosynthesis*
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Estrogen Receptor alpha / genetics
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Female
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Gene Expression Regulation
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Gene Expression Regulation, Neoplastic
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Hyperplasia
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Mammary Glands, Animal / metabolism
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Mammary Glands, Animal / pathology
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Mammary Neoplasms, Experimental / genetics
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Mammary Neoplasms, Experimental / metabolism*
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic
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RNA, Messenger / biosynthesis
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RNA, Messenger / genetics
Substances
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Estrogen Receptor alpha
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RNA, Messenger
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Cyclin D1
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Estradiol