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

  • H. Rubin
  • Kang Xu
Part of the Basic Life Sciences book series (BLSC, volume 57)

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.

Keywords

Label Cell Epigenetic Change Epigenetic Event Focus Formation Chromosome Recombination 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Abbreviations

MCDB 402

molecular, cellular and developmental biology medium 402

CS

calf serum

FBS

fetal bovine serum

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References

  1. 1.
    T. T. Puck, Roundtable: Definition of criteria to define a genetic event, in: “Banbury Report 2. Mammalian Mutagenesis: The Maturation of Test Systems,” Cold Spring Harbor Laboratory, Cold Spring Harbor (1979).Google Scholar
  2. 2.
    P. A. Jacobs, M. Brunton, W. M. Court Brown, R. Doll, and R. Goldstein, Change of human chromosome count distributions with age: Evidence for a sex difference, Nature 197:1080–1081 (1963).PubMedCrossRefGoogle Scholar
  3. 3.
    D. T. Hughes, Cytogenetical polymorphism and evolution in mammalian somatic cell populations in vivo and in vitro, Nature 217:518–523 (1968).PubMedCrossRefGoogle Scholar
  4. 4.
    J. R. Shapiro, W.-K. A. Yung, and W. R. Shapiro, Isolatin, karyotype and clonal growth of heterogeneous subpopulations of human malignant gliomas, Cancer Res. 41:2349–2359 (1981).PubMedGoogle Scholar
  5. 5.
    S. R. Wolman, T. F. Phillips, and F. F. Becker, Fluorescent banding patterns of rat chromosomes in normal cells and primary hepatocellular carcinomas, Science 175:1267–1269 (1972).PubMedCrossRefGoogle Scholar
  6. 6.
    M. Terzi, Chromosomal variation and the establishment of somatic cell lines in vitro, Nature 253:361–362 (1975).PubMedCrossRefGoogle Scholar
  7. 7.
    L. S. Cram, M. F. Bartholdi, A. F. Ray, G. L. Travis, and P. M. Kraemer, Spontaneous neoplastic evolution of Chinese hamster cells in culture: Multistep progression of karyotype, Cancer Res. 43:4828–4837 (1983).PubMedGoogle Scholar
  8. 8.
    J. D. Rowley, Biological implications of consistent chromosomal rearrangements in leukemia and lymphoma, Cancer Res. 44:3159–3168 (1984).PubMedGoogle Scholar
  9. 9.
    C. H. Waddington, “The Strategy of the Genes: A Discussion of Some Aspects of Theoretical Biology”, Allen and Unwin, London (1957).Google Scholar
  10. 10.
    D. L. Nanney, Epigenetic control systems, Proc. Natl. Acad. Sci. USA 44:712–717 (1958).PubMedCrossRefGoogle Scholar
  11. 11.
    D. L. Nanney, Molecules and morphologies: The perpetuation of pattern in the ciliated protozoa, J. Protozool. 24:27–35 (1977).PubMedGoogle Scholar
  12. 12.
    D. A. Clayton, Transcription of the mammalian mitochondrial genome, Ann. Rev. Biochem. 53:573–594 (1984).PubMedCrossRefGoogle Scholar
  13. 13.
    T. J. King and R. Briggs, Serial transplantation of embryonic nuclei, Cold Spring Harbor Symposia Quant. Biol. 21:271–290 (1956).CrossRefGoogle Scholar
  14. 14.
    H. E. Varmus, The molecular genetics of cellular oncogenes, Ann. Rev. Genet. 18:553–612 (1984).PubMedCrossRefGoogle Scholar
  15. 15.
    S. Mondai and C. Heidelberger, In vitro malignant transformation by methylcholanthrene of the progeny of single cells derived from C3H mouse prostate, Proc. Natl. Acad. Sci. USA 65:219–229 (1970).CrossRefGoogle Scholar
  16. 16.
    A. R. Kennedy, M. Fox, G. Murphy, and J. B. Little, Relationship between X-ray exposure and malignant transformation in C3H 10T1/2 cells, Proc. Natl. Acad. Sci. USA 77:7262–7266 (1980).PubMedCrossRefGoogle Scholar
  17. 17.
    A. R. Kennedy, J. Cairns, and J. B. Little, Timing of the steps in transformation of C3H 10T1/2 cells by x-irradiation, Nature 307:85–86 (1984).PubMedCrossRefGoogle Scholar
  18. 18.
    F. Seilern-Aspang and K. Kratochwil, Relation between regeneration and tumor growth, in: “Regeneration in Animals and Related Problems,” V. Kiortsis and H. Trampusch, eds., North Holland, Amsterdam (1965).Google Scholar
  19. 19.
    B. Mintz and K. Illmensee, Normal genetically mosaic mice produced from malignant teratocarcinoma cells, Proc. Natl. Acad. Sci. USA 72:3585–3589 (1975).PubMedCrossRefGoogle Scholar
  20. 20.
    M. Oshimura, D. J. Fitzgerald, H. Kitamura, P. Nettesheim, and J. C. Barrett, Cytogenetic changes in rat tracheal epithelial cells during early stages of carcinogen-induced neoplastic progression, Cancer Res. 48:702–708 (1988).PubMedGoogle Scholar
  21. 21.
    J. L. Jainchill, S. A. Aaronson, and G. J. Todaro, Murine sarcoma and leukemia viruses: assay using clonal lines of contact-inhibited mouse cells, J. Virol. 4:549–553 (1969).PubMedGoogle Scholar
  22. 22.
    G. D. Shipley and R. G. Ham, Attachment and growth of Swiss and Balb/c 3T3 cells in a completely serum-free medium, In Vitro 16:218 (1980).Google Scholar
  23. 23.
    H. Rubin, B. M. Chu, and P. Arnstein, Dynamics of tumor growth and cellular adaptation after inoculation into nude mice of varying number of transformed 3T3 cells and of readaptation to culture of the tumor cells, Cancer Res. 46:2027–2034 (1986).PubMedGoogle Scholar
  24. 24.
    T. Gurney, Local stimulation of growth in primary cultures of chick embryo fibroblasts, Proc. Natl. Acad. Sci. USA 62:906–911 (1969).PubMedCrossRefGoogle Scholar
  25. 25.
    R. Fleischmajer and R. E. Billingham, eds. “Epithelial-Mesenchymal Interactions,” The Williams and Wilkins Company, Baltimore (1968).Google Scholar
  26. 26.
    R. E. Scott, B. J. Hoerl, J. J. Wille, Jr., D. L. Florine, B. R. Krawisz, and K. Yun, Coupling of proadipocyte growth arrest and differentiation II. A cell cycle model for the physiological control of cell proliferation, J. Cell. Biol. 94:400–405 (1982).PubMedCrossRefGoogle Scholar
  27. 27.
    D. I. DePomerai, F.-H. Kotecha, C. Fullick, A. Young, and M. A. H. Gali, Expression of differentiation markers by chick embryo neuroretinal cells in vivo and in culture, J. Embryol. Exp. Morph. 77:201–220 (1983).Google Scholar
  28. 28.
    P. R. Cline and R. H. Rice, Modulation of involucrin and envelope competence in human keratinocytes by hydrocortisone, retinyl acetate and growth arrest, Cancer Res. 43:3203–3207 (1983).PubMedGoogle Scholar
  29. 29.
    D. A. Haber, D. A. Fox, W. S. Dynan, and W. G. Thilly, Cell density dependence of focus formation in the C3H 10T1/2 transformation assay, Cancer Res. 37:1644–1648 (1982).Google Scholar
  30. 30.
    J. S. Bertram, Effects of serum concentration on the expression of carcinogen-induced transformation in the C3H/10T1/2 CL8 cell line, Cancer Res. 37:514–523 (1977).PubMedGoogle Scholar
  31. 31.
    W. F. Benedict, W. L. Wheatley, and P. A. Jones, Inhibition of chemically induced morphological transformation and reversion of the transformed phenotype by ascorbic acid in C3H 10T1/2 cells, Cancer Res. 40:2796–2801 (1980).PubMedGoogle Scholar
  32. 32.
    E. Farber, Pre-cancerous steps in carcinogenesis: Their physiological adaptive nature, Biochim. Biophys. Acta 738:171–180 (1984).PubMedGoogle Scholar
  33. 33.
    E. Farber and D. S. R. Sarma, Biology of disease. Hepatocarcinogenesis: A dynamic cellular perspective, Lab. Invest. 56:4–22 (1987).PubMedGoogle Scholar
  34. 34.
    D. G. Blair, C. S. Cooper, M. K. Oskarsson, L. A. Eader, and G. F. Vande Woude, New method for detecting cellular transforming genes, Science 218:1122–1124 (1982).PubMedCrossRefGoogle Scholar
  35. 35.
    M. A. Tainsky, F. L. Shamansky, D. Blair, and G. Vande Woude, Human recipient cell for oncogene transfection studies, Mol. Cell. Biol. 7:1280–1284 (1987).PubMedGoogle Scholar
  36. 36.
    R. G. Greig, T. P. Koestler, D. L. Trainer, S. P. Corwin, L. Miles, T. Kline, R. Sweet, S. Yokoyama, and G. Poste, Tumorigenic and metastatic properties of “normal” and ras-transformed NIH 3T3 cells, Proc. Natl. Acad. Sci. USA 82:3698–3701 (1985).PubMedCrossRefGoogle Scholar
  37. 37.
    W. M. Elsasser, Reflections on a theory of organisms, Éditions Orbis Publishing, Frelighsburg (1987).Google Scholar
  38. 38.
    A. Eddington, “The Philosophy of Science,” reprinted by the University of Michigan Press, Ann Arbor (1939).Google Scholar
  39. 1.
    Science, 188:68-70 (1975).Google Scholar
  40. 2.
    Cancer Res. 36:1626-1633, (1976).Google Scholar
  41. 3.
    J. Supramolecular Structure 5:131-137 (1976).Google Scholar

Copyright information

© Plenum Press, New York 1991

Authors and Affiliations

  • H. Rubin
    • 1
  • Kang Xu
    • 1
  1. 1.Department of Molecular Biology and Virus LaboratoryUniversity of CaliforniaBerkeleyUSA

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