Frech M Silvina, Halama Ewa D, Tilli Maddalena T, Singh Baljit, Gunther Edward J, Chodosh Lewis A, Flaws Jodi A, Furth Priscilla A
Lombardi Comprehensive Cancer Center, Departments of Oncology and Pathology, Georgetown University, 3970 Reservoir Road, Washington, DC 20057, USA.
Cancer Res. 2005 Feb 1;65(3):681-5.
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.
一种在乳腺上皮细胞中雌激素受体α表达失调的条件性四环素反应性转基因小鼠模型,在4月龄时出现了导管增生(DH)、小叶增生和原位导管癌(DCIS)。在正常和异常的导管及小叶结构中均发现了较高的增殖率。DH和DCIS而非正常导管结构显示核定位细胞周期蛋白D1的细胞百分比增加。在外源性17β-雌二醇处理后,这些表型的发生率或程度均未发现差异,这表明ERα表达的改变是DH、小叶增生和DCIS发生的限速因素。