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Ribosomal Protein S6 Kinase and PKC in Human Mammary Tumor Cells

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Endocrine Therapy and Growth Regulation of Breast Cancer

Part of the book series: Recent Results in Cancer Research ((RECENTCANCER,volume 113))

Abstract

It is well established that 17-β estradiol (E2) influences the growth of human breast cancer (Patterson et al. 1982; Edwards et al. 1979; Maass and Jonat 1983; Howat et al. 1985), but it is unclear wheter E2 acts directly or indirectly on the proliferation of target cells (Soto and Sonnenschein 1987; Dickson and Lippman 1987; King 1985). At present, there is increasing evidence that polypeptide growth factors (GF) also regulate the growth of human breast cancer (Dickson and Lippman 1987; King 1985; Dickson et al. 1986; Dickson et al. 1986). Therefore, E2 may in part promote the growth through the regulation of autostimulatory and autoinhibitory GFs (Soto and Sonnenschein 1987; Dickson and Lippman 1987; Knabbe et al. 1987). Consequently, the hormone dependency of breast tumor cells may be limited not only to functional estrogen receptors (ER) but also to functional growth factor receptors (GF-R). Such GF-Rs are likely to represent important growth-regulatory elements in the estrogen-induced autocrine or paracrine growth mechanisms of human breast cancer (Fitzpatrick et al. 1984; Macias et al. 1986; Sainsbury et al. 1985; Wyss et al. 1987; Sainsbury et al. 1987; Furlanetto and DiCarlo 1984).

This study was supported in part by the Swiss National Foundation Number 3.344–0.86 and the Roche Research Foundation (I. N.).

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© 1989 Springer-Verlag Berlin · Heidelberg

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Fabbro, D., Novak-Hofer, I., Küng, W., Meyer, T., Matter, A., Eppenberger, U. (1989). Ribosomal Protein S6 Kinase and PKC in Human Mammary Tumor Cells. In: Eppenberger, U., Goldhirsch, A. (eds) Endocrine Therapy and Growth Regulation of Breast Cancer. Recent Results in Cancer Research, vol 113. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-83638-1_6

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  • DOI: https://doi.org/10.1007/978-3-642-83638-1_6

  • Publisher Name: Springer, Berlin, Heidelberg

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