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• W118909215 abstract "Estrogen is a major regulator of mammary gland development and function, and affects the growth and progression of mammary cancers (1,2). In particular, the growth responsiveness of breast cancer (BC) cells to estrogen is the basic rationale for the efficacy of the so-called endocrine therapies, such as antiestrogens. Estrogens mediate their action via the estrogen receptor (ER), which belongs to the steroid/thyroid/retinoid receptor gene superfamily (3). The protein products of this family are intracellular, ligand-activated transcription factors regulating the expression of several gene products, which ultimately elicit a target tissue-specific response (4). Indeed, ER, together with progesterone receptor (PR), expression in human breast tumors, are important prognostic indicators, as well as markers of responsiveness to endocrine therapies (5, 6). However, although the majority of human BCs are thought to be initially hormone-responsive, it is well appreciated that alterations in responsiveness to estrogen occurs during breast tumorigenesis. During BC progression, some ER-positive BCs are de novo resistant to endocrine therapies, and of those that originally respond to antiestrogens, many develop resistance. This progression from hormonal dependence to independence is a significant clinical problem, because it limits the useful of the relatively nontoxic endocrine therapies, and is associated with a more aggressive disease phenotype (7). This occurs despite the continued expression of ER, and often PR (8,9). The ER is pivotal in estrogen and antiestrogen action in any target cell, but the nature of the ER is clearly multifaceted." @default.
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• W118909215 date "2000-01-01" @default.
• W118909215 modified "2023-09-28" @default.
• W118909215 title "Multiple Facets of Estrogen Receptor in Human Breast Cancer" @default.
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• W118909215 doi "https://doi.org/10.1007/978-1-59259-223-4_2" @default.
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