Deregulated estrogen receptor alpha expression in mammary epithelial cells of transgenic mice results in the development of ductal carcinoma in situ.
Deregulated estrogen receptor alpha expression in mammary epithelial cells of transgenic mice results in the development of ductal carcinoma in situ.
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DOI：
10.1158/0008-5472.681.65.3
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发表时间：
2005-02
期刊：
影响因子：
11.2
通讯作者：
M. S. Frech;E. Halama;M. Tilli;Baljit Singh;Baljit Singh;E. Gunther;L. Chodosh;J. Flaws;P. Furth
中科院分区：
文献类型：
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作者：
M. S. Frech;E. Halama;M. Tilli;Baljit Singh;Baljit Singh;E. Gunther;L. Chodosh;J. Flaws;P. Furth
乳腺上皮细胞中雌激素受体α表达失调的条件性四环素应答转基因小鼠模型在4月龄时发生导管增生（DH）、小叶增生和导管原位癌（DCIS）。在正常和异常的导管和小叶结构中发现较高的增殖率。DH和DCIS，而不是正常的导管结构显示细胞核定位的细胞周期蛋白D1的百分比增加。外源性17 β-雌二醇治疗后这些表型的患病率或程度无差异，表明ER α表达的改变是DH、小叶增生和DCIS发生的限速因素。
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.