A Relationship between SV40-transformed Cell Susceptibility to Macrophage Killing and Tumor Induction in Rodents

  • James L. Cook
  • John B. HibbsJr.
  • Andrew M. LewisJr.
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 134)

Abstract

Simian virus 40 (SV40) is a papovavirus that induces tumors in golden Syrian hamsters and transforms cells from many species in tissue culture (1). The ability of SV40-transformed hamster cells, but not cells from other species transformed by SV40, to induce tumors in the host (2) implies that in transformation of hamster cells, SV40 may induce a species-specific change that renders the neoplastic cells resistant to rejection by the host. Previous studies by the authors suggested that LSH hamster cells transformed by adenovirus 2 (Ad2, a human virus not oncogenic in newborn hamsters) (3,4) are susceptible to rejection by a thymus-dependent, cell-mediated host response (5,6,7). The resistance of SV40-transformed LSH cells to rejection by syngeneic animals and the recent observation that SV40-transformed LSH cells induce tumors in histoincompatible CB hamsters almost as efficiently as in syngeneic animals (8) support the hypothesis that SV40 alters the efficiency with which the hamster cells it transforms are recognized or destroyed by the host.

Keywords

Agar Rubber Bacillus Resis Peptone 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Butel, J.S. et al. Adv Cancer Res 15 (1972) 1.PubMedCrossRefGoogle Scholar
  2. 2.
    Eddy, B.E. Prog Exp Tumor Res 4 (1964) 1.PubMedGoogle Scholar
  3. 3.
    Trentin, J.J. et al. Science 137 (1962) 835.PubMedCrossRefGoogle Scholar
  4. 4.
    Huebner, R.J. In: Perspectives in Virology, ed. Pollard, Vol.5. Academic Press, New York (1967) 147.Google Scholar
  5. 5.
    Cook, J.L.; Lewis, A.M., Jr. Cancer Res 39 (1979) 1455.PubMedGoogle Scholar
  6. 6.
    Cook, J.L. et al. Cancer Res 39 (1979) 3335.PubMedGoogle Scholar
  7. 7.
    Cook, J.L. et al. Cancer Res 39 (1979) 4949.PubMedGoogle Scholar
  8. 8.
    Lewis, A.M., Jr.; Cook, J.L. Proc Natl Acad Sci 77 (1980) 2286.Google Scholar
  9. 9.
    Hibbs, J.B., Jr. Nature [New Biol] 235 (1972) 48.Google Scholar
  10. 10.
    Hibbs, J.B., Jr. et al. Science 197 (1977) 279.PubMedCrossRefGoogle Scholar
  11. 11.
    Cook, J.L. et al. Proc Natl Acad Sci (in press).Google Scholar
  12. 12.
    Hibbs, J.B., Jr. Science 180 (1973) 868.PubMedCrossRefGoogle Scholar
  13. 13.
    Black, P.H.; Rowe, W.P. Proc Soc Exp Biol Med 114 (1963) 721.PubMedGoogle Scholar
  14. 14.
    Black, P.H.; Rowe, W.P. Proc Natl Acad Sci USA 50 (1963) 606.PubMedCrossRefGoogle Scholar
  15. 15.
    Fidler, I.J. et al. Cell Immunol 38 (1978) 131.PubMedCrossRefGoogle Scholar
  16. 16.
    Tevethia, S.S. et al. In: Immunobiology of the Macrophage, ed. Nelson. Academic Press, New York (1976) 509.Google Scholar
  17. 17.
    Howell, S.B. et al. Int J Cancer 14 (1974) 662.PubMedCrossRefGoogle Scholar
  18. 18.
    Tevethia, S.S. In: Viral Oncology, ed. Klein. Raven Press, New York (1980) 581.Google Scholar
  19. 19.
    Glaser, M. J Exp Med 149 (1979) 774.PubMedCrossRefGoogle Scholar
  20. 20.
    Chen, H. et al. Eur J Immunol 9 (1979) 80.PubMedCrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1981

Authors and Affiliations

  • James L. Cook
    • 1
    • 2
  • John B. HibbsJr.
    • 1
    • 2
  • Andrew M. LewisJr.
    • 1
    • 2
  1. 1.Veterans Administration Hospital and University of Utah Medical CenterSalt Lake CityUSA
  2. 2.National Institute of Allergy and Infectious DiseasesNational Institutes of HealthBethesdaUSA

Personalised recommendations