Introduction

BC is the most common cancer in women worldwide. Attempts at prevention of BC are important areas of clinical and experimental investigations and many different approaches are being used for such studies (1-4). A full term pregnancy before the age of 20 is the only natural phenomenon known that can drastically reduce the risk of BC in women of all ethnic backgrounds worldwide (5-8). This universal protective effect of early pregnancy is clearly of major consideration in devising strategies for BC prevention. Rats that have been exposed to chemical carcinogens before or after undergoing a full-term pregnancy are protected from mammary carcinogenesis (9-15). Mice that undergo a full term pregnancy also have a greatly reduced susceptibility to chemical carcinogen induced mammary carcinogenesis compared to nulliparous animals (16-18).

Hormonal prevention strategies have used exogenous hormonal treatment to mimic the protective effect of pregnancy against BC. High levels of and progesterone (P) given for 30 days beginning 15 days after carcinogen administration inhibited mammary carcinogenesis in Sprague Dawley rats treated with the carcinogens (19,20). Medina (21) also showed that treatment with E2 and P, prior to initiation of cancer cells with a carcinogen was highly protective. Human chorionic gonadotropin treatment either before or after carcinogen exposure induces protection from mammary carcinogenesis (13). Short-term (7-21 days) treatment with pregnancy level of with or without P is highly effective in conferring protection against chemical carcinogen induced carcinogenesis in rats (22, 23).

Despite having strong epidemiological, clinical, and experimental evidences suggesting parity-related or hormone-induced refractoriness against mammary carcinogenesis, very little is known about the physiological and molecular mechanisms governing this parity-induced protection. To understand the molecular bases of the protective effect of hormonal treatment, we analyzed the difference in gene expression levels between the protected and the susceptible states using cDNA microarrays. We used a global approach to identify differences in gene expression patterns that may be useful to establish the efficacy of protective hormone treatment, and as biomarkers for the success or failure of hormone treatments.

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