Background Breast cancer is the selleck chemicals most common type of cancer and the second leading cause of death among women in the United States. The principle therapeutic strategy for breast cancer involves surgical removal of the primary tumor following extensive radiotherapy and chemother apy. Several clinical trials have suggested that estrogen ablation or anti estrogen strategy is effective in the pre vention or treatment of breast cancer, especially in estro Inhibitors,Modulators,Libraries gen receptors dependent breast cancer. There are two major isoforms of ERs that have been identified and the ER isoform is believed to primarily contribute to estrogen induced growth stimu latory effects in breast cancer. Estrogens binding to ERs result in activated signaling pathways leading to cel lular proliferation and differentiation in normal mam mary tissue.

However, aberrant activation of estrogen Inhibitors,Modulators,Libraries ER signaling renders unlimited and uncontrolled Inhibitors,Modulators,Libraries cell prolif eration which occurs in most breast tumors. The estrogen antagonist, tamoxifen, is currently the first line medical treatment for ER positive breast can cer at all stages of this disease in both pre and postme nopausal women. TAM has also been shown to have potential benefit for the prevention of breast cancer among women at high risk of breast cancer. How ever, ER negative breast cancers do not respond to TAM treatment and generally have a more clinically ag gressive progression resulting in a poorer prognosis. Extensive studies have shown that the major cause for inactive ER signaling is the absence of ER gene ex pression.

Although the precise mechanisms of ER tran scription regulation are still under investigation, it has been clear that acquired loss Inhibitors,Modulators,Libraries of ER transcription rather than a genetic alteration such as DNA mutations is a potential mechanism for hormone resistance in ER negative breast cancer. Inhibitors,Modulators,Libraries Recent studies indicate that epigenetic mechanisms, which primarily involve two path ways, DNA methylation and histone modification, may play a crucial role in regulating ER expression. Supportive evidence has included intervention application of epigenetic modulators such as DNA methyltranferase inhibitor, 5 aza 2 deoxycytidine, and his tone deacetylase inhibitor, trichostatin A, which successfully induced ER expression and sensitized hormone resistant ER negative breast cancer cells to chemotherapy.

In this regard, it is increasingly evi selleck bio dent that epigenetic events play an important role in ER gene expression. Despite a high incidence and mortality by breast can cer in the United States and Europe, Asian women who consumed 20 50 times more soy products per capita than their western counterparts have much less suscepti bility to developing breast cancer. Soybean prod uct is a rich source of genistein isoflavone, which is believed to be a potent botanical chemopreventive com pound against various types of cancers, including breast cancer.