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Reduction of Nuclear Oncogene Expression by Endogenous and Exogenous Interferons

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Interferons in Oncology

Part of the book series: ESO Monographs ((ESO MONOGRAPHS))

Abstract

The regulation of the c-myc nuclear oncogene and its role in the malignant transformation of cells have been studied extensively during the past years (for a general review consult ref. 1). The expression of c-myc is characteristic of normal proliferating cells and this gene is one of the downstream targets along the mitogenic pathway initiated by growth factors (4–7). On the other hand, the c-myc gene is selectively switched off when cells enter the quiescent, non-proliferative state (G0/G1 phase) that accompanies terminal differentiation. It is clear, from many studies, that, in order to understand the nature of abnormal activation of c-myc gene in tumor cells, it is important to understand first how the gene is normally regulated and suppressed in the growth arrested cells. During the past few years we have developed a concept according to which natural growth inhibitors could be used to analyse the control intracellular elements which switch off the c-myc gene. Although the chalone concept which predicts the existence of growth inhibitory substances was developed a long time ago (8), only a few naturally occurring polypeptides which inhibit cellular proliferation have been completely identified and characterized so far. In this respect, the group of interferons (IFNs), the beta-transforming growth factor and tumor necrosis factor (TNF) represent the first well-defined highly potent polypeptides which exert antimitogenic effects on cells (9–13).

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© 1987 Springer-Verlag Berlin Heidelberg

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Kimchi, A. (1987). Reduction of Nuclear Oncogene Expression by Endogenous and Exogenous Interferons. In: Smyth, J.F. (eds) Interferons in Oncology. ESO Monographs. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-72805-1_7

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  • DOI: https://doi.org/10.1007/978-3-642-72805-1_7

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-72807-5

  • Online ISBN: 978-3-642-72805-1

  • eBook Packages: Springer Book Archive

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