Abstract
Extended exposure to the selective estrogen receptor modulators (SERMs) such as raloxifene to prevent osteoporosis and tamoxifen or the aromatase inhibitors to treat or prevent breast cancer are established therapeutic strategies. However, there are now clearly defined consequences of exhaustive antihormonal therapy in breast cancer. Ultimately, drug resistance to SERMs and aromatase inhibitors enhances cancer cell survival but a paradoxical supersensitivity to estrogen action develops that causes cancer cell apoptosis. The future exploitation of these novel data will allow selective killing of cancer with fewer side effects for patients.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Apoptosis / physiology
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Breast Neoplasms / drug therapy
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Breast Neoplasms / metabolism*
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Dimerization
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Drug Resistance
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Endometrial Neoplasms / drug therapy
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Endometrial Neoplasms / metabolism
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Estrogen Antagonists
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Estrogen Receptor Modulators / metabolism
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Estrogen Receptor Modulators / pharmacology*
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Estrogen Replacement Therapy
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Estrogens / metabolism*
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Female
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Hot Flashes / chemically induced
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Humans
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Osteoporosis / chemically induced
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Protein Binding
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Protein Conformation
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Protein Interaction Mapping
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Raloxifene Hydrochloride / adverse effects
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Raloxifene Hydrochloride / pharmacology
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Receptors, Estrogen / antagonists & inhibitors
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Receptors, Estrogen / metabolism*
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Signal Transduction
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Tamoxifen / adverse effects
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Tamoxifen / pharmacology
Substances
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Estrogen Antagonists
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Estrogen Receptor Modulators
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Estrogens
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Receptors, Estrogen
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Tamoxifen
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Raloxifene Hydrochloride