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The study of epigenetic regulation of genes involved in breast cancer provides a level of complexity that lends understanding to the factors contributing to this prevalent disease. Recent evidence from studies that employ pharmacological agents such as trichostatin A and/or 5-aza-cytidine to alter epigenetic changes have been shown to reactivate key regulators such as p21 in breast cancer cells or explain silencing mechanisms of p16 that could lead to carcinogenesis. The roles of telomerase and Bmi-1 expression in the cellular processes of senescence, aging, and the maintenance of stem cells are discussed in relation to breast carcinogenesis, the implications of breast cancer stem cells, and the feasibility of these genes as epigenetic targets in cancer therapy.