Abstract
Estrogenic hormones are known to stimulate a variety of biosynthetic processes in hormone-responsive target cells, such as those of the breast and uterus, and nonsteroidal antiestrogens have been shown to antagonize many of the actions of estrogens (1–3). Indeed, antiestrogens have proven to be effective in controlling the growth of estrogen-responsive breast cancers (4). The actions of estrogens appear to be mediated via interaction with an intracellular receptor protein (5–7). Ligand-free estrogen receptors are weakly associated with nuclear components. Following ligand binding, receptor complexes become tightly associated with specific nuclear components, and this association presumably alters gene expression (8–10). Antiestrogens also bind directly to the estrogen receptor, and the resulting antiestrogen-receptor complexes also become associated with chromatin, but presumably block the events which promote cell growth (11,12).
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© 1988 Plenum Press, New York
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Katzenellenbogen, B.S., Sheen, Y.Y., Snider, C.E., Berthois, Y. (1988). Estrogen and Antiestrogen Regulation of Proliferation and Protein Synthesis of Human Breast Cancer Cells. In: Moudgil, V.K. (eds) Steroid Receptors in Health and Disease. Serono Symposia, USA. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5541-0_15
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DOI: https://doi.org/10.1007/978-1-4684-5541-0_15
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