Deregulated estrogen receptor α expression in mammary epithelial cells of transgenic mice results in the development of ductal carcinoma In situ

M. Silvina Frech; Ewa D. Halama; Maddalena T. Tilli; Baljit Singh; Edward J. Gunther; Lewis A. Chodosh; Jodi A. Flaws; Priscilla A. Furth

Deregulated estrogen receptor α expression in mammary epithelial cells of transgenic mice results in the development of ductal carcinoma In situ

M. Silvina Frech, Ewa D. Halama, Maddalena T. Tilli, Baljit Singh, Edward J. Gunther, Lewis A. Chodosh, Jodi A. Flaws, Priscilla A. Furth

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Abstract

A conditional tetracycline-responsive transgenic mouse model with deregulated estrogen receptor α expression in mammary epithelial cells developed ductal hyperplasia (DH), Iobular 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 17β-estradiol treatment were found suggesting that alteration of ERα expression was the rate-limiting factor in initiation of DH, lobular hyperplasia, and DCIS.

Original language	English (US)
Pages (from-to)	681-685
Number of pages	5
Journal	Cancer Research
Volume	65
Issue number	3
State	Published - Feb 1 2005

All Science Journal Classification (ASJC) codes

Oncology
Cancer Research

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title = "Deregulated estrogen receptor α expression in mammary epithelial cells of transgenic mice results in the development of ductal carcinoma In situ",

abstract = "A conditional tetracycline-responsive transgenic mouse model with deregulated estrogen receptor α expression in mammary epithelial cells developed ductal hyperplasia (DH), Iobular 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 17β-estradiol treatment were found suggesting that alteration of ERα expression was the rate-limiting factor in initiation of DH, lobular hyperplasia, and DCIS.",

author = "Frech, {M. Silvina} and Halama, {Ewa D.} and Tilli, {Maddalena T.} and Baljit Singh and Gunther, {Edward J.} and Chodosh, {Lewis A.} and Flaws, {Jodi A.} and Furth, {Priscilla A.}",

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language = "English (US)",

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T1 - Deregulated estrogen receptor α expression in mammary epithelial cells of transgenic mice results in the development of ductal carcinoma In situ

AU - Frech, M. Silvina

AU - Halama, Ewa D.

AU - Tilli, Maddalena T.

AU - Singh, Baljit

AU - Gunther, Edward J.

AU - Chodosh, Lewis A.

AU - Flaws, Jodi A.

AU - Furth, Priscilla A.

PY - 2005/2/1

Y1 - 2005/2/1

N2 - A conditional tetracycline-responsive transgenic mouse model with deregulated estrogen receptor α expression in mammary epithelial cells developed ductal hyperplasia (DH), Iobular 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 17β-estradiol treatment were found suggesting that alteration of ERα expression was the rate-limiting factor in initiation of DH, lobular hyperplasia, and DCIS.

AB - A conditional tetracycline-responsive transgenic mouse model with deregulated estrogen receptor α expression in mammary epithelial cells developed ductal hyperplasia (DH), Iobular 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 17β-estradiol treatment were found suggesting that alteration of ERα expression was the rate-limiting factor in initiation of DH, lobular hyperplasia, and DCIS.

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Deregulated estrogen receptor α expression in mammary epithelial cells of transgenic mice results in the development of ductal carcinoma In situ

Abstract

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