Abstract
Abstract A full term pregnancy early in life reduces the risk of breast cancer in women. A similar phenomenon is also observed in rats and mice. Short-term treatment with pregnancy levels of estradiol is also highly effective in preventing mammary carcinogenesis. In the current study our objective was to determine whether short-term treatment with pregnancy levels of estradiol conferred protection against mammary carcinogenesis by blocking initiation or promotion. Rats were injected with N-methyl-N-nitrosourea at 7 weeks of age and treated with 20 µg, 100 µg, 200 µg or 30 mg of estradiol in silastic capsules for 3-weeks. The experiments were terminated 9 months post carcinogen treatment. Mammary gland wholemounts were prepared at termination and examined for the presence of latent microscopic mammary cancers. Short-term treatment with pregnancy levels of estradiol drastically reduced the incidence of overt mammary cancers. 100 µg, 200 µg and 30 mg doses of estradiol resulted in levels of estradiol equivalent to pregnancy level and were effective in preventing overt mammary cancer incidence compared to control or 20 µg estradiol treatment which did not result in pregnancy levels of estradiol in the circulation. Although a significant reduction of overt cancers was observed in the pregnancy levels of estradiol treated groups, there was no difference in the incidence of microscopic mammary cancers between the estradiol treated and the controls. Proliferation of microscopic mammary cancers was examined using immunohistochemistry for cyclin D1 expression. Proliferation in the microscopic mammary cancers of the protected groups was significantly lower (∼ 2-3 fold) than the microscopic mammary cancers in the unprotected groups. These findings clearly demonstrate that short-term treatment with pregnancy levels of estradiol confers protection against mammary cancer development by blocking promotion and progression of carcinogen initiated cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 571. doi:1538-7445.AM2012-571
Published Version
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