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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Rat strain-specific actions of 17β-estradiol in the mammary aland: correlation between estroaen- induced lobuloalveolar hyperplasia and susceptibility to estrogen-induced mammary cancers
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Rat strain-specific actions of 17β-estradiol in the mammary aland: correlation between estroaen- induced lobuloalveolar hyperplasia and susceptibility to estrogen-induced mammary cancers

机译：大鼠乳腺中17β-雌二醇的大鼠品系特异性作用：雌激素诱导的小叶肺泡增生与对雌激素诱导的乳腺癌的敏感性之间的相关性

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摘要

The genetically related ACl and Copenhagen (COP) rat strains display diametrically opposed susceptibilities to mammary cancer development when treated chronically with 17β-estradiol (E2). Here, we compare the actions of E2 on cell proliferation and lobuloalveolar development in the mammary glands of female ACl and COP rats. After 12 wk of E2 treatment. the mammary glands of ACl rats exhibited a significantly greater proliferative response to EZ, compared with COP rats, as evidenced by quantification of S phase fraction and development of lobuloalveolar hyperplasia. Focal regions of atypical epithelial hyperplasia were observed in ACl. but not COP, rats. These strain differences were not because of differences in circulating E2, progesterone or. prolactin. Two- thirds of the induced mammary cancers in ACl rats exhibited aneuploidy. The E2-induced mammary cancers regressed when hormone treatment was discontinued. indicating that they were estrogen-dependent. Progesterone receptor was expressed by the great majority of epithelial cells within the E2-induced atypical hyperplastic foci and the mammary carcinomas, suggesting a link between these lesions. These data demonstrate a correlation between E2 action in the induction of mammary cell proliferation and atypical epithelial hyperplasia and genetically conferred sus- ceptibility to E2-induced mammary cancers.
机译：遗传相关的ACl和Copenhagen（COP）大鼠品系长期用17β-雌二醇（E2）治疗后，对乳腺癌的发展表现出截然相反的敏感性。在这里，我们比较E2对雌性ACl和COP大鼠乳腺中细胞增殖和小叶肺泡发育的作用。 E2处理12周后。与COP大鼠相比，ACl大鼠的乳腺对EZ表现出明显更大的增殖反应，这可以通过S期分数的定量和小叶肺泡增生的发展来证明。在ACl中观察到非典型上皮增生的焦点区域。但不是COP，老鼠。这些菌株的差异不是由于循环中的E2，孕酮或雌激素的差异。催乳素。 ACl大鼠中三分之二的诱发乳癌表现出非整倍性。当激素治疗中断时，E2诱导的乳腺癌会消退。表明它们是雌激素依赖性的。孕酮受体由E2诱导的非典型增生灶和乳腺癌中的绝大多数上皮细胞表达，提示这些病变之间存在联系。这些数据表明，E2在诱导乳腺细胞增生和非典型上皮增生中的作用与遗传赋予的对E2诱导的乳腺癌的敏感性之间存在相关性。

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