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Expression in Mammary Epithelial Cells of Transgenic Mice Results in the Development of Ductal Carcinoma In situ
1 Lombardi Comprehensive Cancer Center, Departments of 2 Oncology and 3 Pathology, Georgetown University, Washington, District of Columbia; 4 Department of Cancer Biology and Abramson Family Cancer Research Institute, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania; and 5 Department of Epidemiology and Preventive Medicine, School of Medicine, University of Maryland, Baltimore, Maryland
Requests for reprints: Priscilla A. Furth, Georgetown University, Research Building, Room E520A, 3970 Reservoir Road, Washington, DC 20057. Phone: 202-687-4437; Fax: 202-687-7505; E-mail: paf3{at}georgetown.edu..
A conditional tetracycline-responsive transgenic mouse model with deregulated estrogen receptor 
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 17ß-estradiol treatment were found suggesting that alteration of ER expression was the rate-limiting factor in initiation of DH, lobular hyperplasia, and DCIS.
Key Words: ER • mammary gland • DCIS • tetracycline responsive gene expression • transgenic mice
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