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Epigenetic Features of Spontaneous Transformation in the NIH 3T3 Line of Mouse Cells

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Boundaries between Promotion and Progression during Carcinogenesis

Part of the book series: Basic Life Sciences ((BLSC,volume 57))

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Abstract

There is a longstanding debate in cancer research about the primary cause of malignant cell growth: is cancer the result of genetic events or the outcome of epigenetic processes? The weight of opinion seems to shift with research trends of biology in general. It is, of course, central to the resolution of such a problem that the concepts at issue be defined. Genetic events are of two basic kinds, mutation and chromosome recombination. Mutations result from a change in the sequence of nucleotides in DNA. They are generally assumed to occur at random with a frequency of less than 10−6 per cell division with little or no evidence of specificity1. Chromosome recombination normally occurs in an orderly way in sexual reproduction. It also occurs in disorderly fashion in somatic cells of aging individuals2,3, in tumors4,5 and in cell culture6,7. Except for certain leukemias8, abnormalities in cell chromosome structure or number in common adult cancers show little evidence of a specific causal relation to the origin of the tumor. However, genetic change is conceptually simple and has been vigorously analyzed in this area of molecular biology. Concurrently, there has been a strong shift toward acceptance of genetic change in somatic cells as the cause of most cancers, and at least part of this shift stems from the combination of conceptual simplicity plus the availability of a highly developed molecular technology for genetic analysis.

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Abbreviations

MCDB 402:

molecular, cellular and developmental biology medium 402

CS:

calf serum

FBS:

fetal bovine serum

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© 1991 Plenum Press, New York

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Rubin, H., Xu, K. (1991). Epigenetic Features of Spontaneous Transformation in the NIH 3T3 Line of Mouse Cells. In: Sudilovsky, O., Pitot, H.C., Liotta, L.A. (eds) Boundaries between Promotion and Progression during Carcinogenesis. Basic Life Sciences, vol 57. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5994-4_25

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  • DOI: https://doi.org/10.1007/978-1-4684-5994-4_25

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4684-5996-8

  • Online ISBN: 978-1-4684-5994-4

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