In 1976, Sporn has defined chemoprevention as ââ?¬Å?the use of pharmacologic or natural agents that inhibit the development of\r\ninvasive breast cancer either by blocking the DNA damage that initiates carcinogenesis, or by arresting or reversing the progression\r\nof premalignant cells in which such damage has already occurred.ââ?¬Â Although the precise mechanism or mechanisms that promote\r\na breast cancer are not completely established, the success of several recent clinical trials in preventive settings in selected highrisk\r\npopulations suggests that chemoprevention is a rational and an appealing strategy. Breast cancer chemoprevention has focused\r\nheavily on endocrine intervention using selective estrogen receptor modulators (SERMs) and aromatase inhibitors (AIs). Achieving\r\nmuch success in this particular setting and new approaches as low-dose administration are actually under investigations in several\r\ntopics. Unfortunately, these drugs are active in prevention of endocrine responsive lesions only and have no effect in reducing\r\nthe risk of estrogen-negative breast cancer. Thus, recently new pathways, biomarkers, and agents likely are to be effective in this\r\nsubgroup of cancers and were put under investigation. Moreover, the identification of new potential molecular targets and the\r\ndevelopment of agents aimed at these targets within cancer have already had a significant impact on advanced cancer therapy\r\nand provide a wealth of opportunities for chemoprevention. This paper will highlight current clinical research in both ERpositive\r\nand ER-negative breast cancer chemoprevention, explaining the biologic effect of the various agents on carcinogenesis and\r\nprecancerous lesions, and finally presenting an excursus on the state-of-the-art about new molecular targets under investigations\r\nin breast cancer settings.
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