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The Cell Cycle and Tumorigenesis in Plants

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Cell Cycle and Cell Differentiation

Part of the book series: Results and Problems in Cell Differentiation ((RESULTS,volume 7))

Abstract

The experimental oncologist is interested in persistently dividing cells and in discovering the reason why tumor cells divide continuously in their hosts while the growth of all normal cells is precisely regulated. The development by tumor cells of a capacity for essentially unrestrained or autonomous growth is the essential feature that characterizes the tumorous state for without it there would be no tumors. It is therefore clear that an understanding of those substances and mechanisms that regulate normal cell growth and division is important if insight is to be gained into how those regulatory mechanisms are affected when a cell is transformed to the neoplastic state. Other clinically important characteristics, such as, for example, the ability of certain tumor cells to invade and metastasize, may be acquired, sometimes relatively late, and can therefore be dismissed in a search for the earliest events that lead to the establishment and maintenance of the tumorous state.

Certain of these studies were supported in part by a research grant (PHS CA-13808 from the National Cancer Institute, U.S. Public Health Service.

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Authors and Affiliations

  1. The Rockefeller University, New York, NY, USA

    Armin C. Braun

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  1. Armin C. Braun
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Editors and Affiliations

  1. Department of Anatomy, University of Pennsylvania, Philadelphia, Pennsylvania, USA

    Howard Holtzer

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© 1975 Springer-Verlag Berlin Heidelberg

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Braun, A.C. (1975). The Cell Cycle and Tumorigenesis in Plants. In: Reinert, J., Holtzer, H. (eds) Cell Cycle and Cell Differentiation. Results and Problems in Cell Differentiation, vol 7. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-37390-2_10

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  • DOI: https://doi.org/10.1007/978-3-540-37390-2_10

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-662-21693-4

  • Online ISBN: 978-3-540-37390-2

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