Part of the book series: Cancer Treatment and Research ((CTAR,volume 83))

Abstract

Estrogens function as mitogens primarily in the G1 phase of the cell cycle by recruiting cells into the cycle and by shortening the length of their G1 phase. Conversely, estrogen antagonists that inhibit cell proliferation reduce the proportion of cells in S phase [1]. The precise role of estrogen in cell growth and proliferation is poorly understood. Initially it was proposed that estrogens stimulate proliferation indirectly by increasing the production of growth factors such as transforming growth factor (TGF)- α [2] or reducing the secretion of growth inhibitory factors such as TGF-β [3,4]. Alternatively, since estrogens stimulate the expression of receptors for a number of growth factors, including those for insulin-like growth factor (IGF-I) and epidermal growth factor (EGF) [5,6], they might function by increasing the sensitivity of cells to growth factors produced either by tumor cells themselves or perhaps by surrounding stromal cells, thereby regulating cell proliferation by a paracrine mechanism [7].

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© 1996 Kluwer Academic Publishers

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Parker, M.G. (1996). Antiestrogen-estrogen receptor interactions. In: Dickson, R.B., Lippman, M.E. (eds) Mammary Tumor Cell Cycle, Differentiation, and Metastasis. Cancer Treatment and Research, vol 83. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1259-8_11

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  • DOI: https://doi.org/10.1007/978-1-4613-1259-8_11

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4612-8536-6

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