Conclusions

Our results indicate that short-term treatment with any dose of E2 that results in serum levels equivalent to the high levels of E2 during the third week of pregnancy are able to confer persistent protection from chemical carcinogen induced mammary carcinogenesis in rats.

Our goal is to use the rodent model system to develop a safe, efficient mechanism based, short-term hormonal intervention for protection from mammary carcinogenesis that can serve as an experimental paradigm for developing BC prevention strategies for women. We hypothesize that short-term treatment with high pregnancy levels of or parity confers protection from mammary carcinogenesis by causing persistent alterations in the hypothalmo-pituitary axis resulting in a decrease in the blood levels ofthe mammogenic hormones, prolactin and growth hormone, causing a reduction in the promotion of carcinogen initiated mammary cells to frank mammary cancers

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