Cooperative Interactions Involving Cellular and Viral Oncogenes in the Development of Malignant Tumors

  • Evelyne Mougneau
  • Christa Cerni
  • Francois Cuzin
Conference paper
Part of the Veröffentlichungen aus der Geomedizinischen Forschungsstelle der Heidelberger Akademie der Wissenschaften book series (HD AKAD, volume 1987/88 / 1987/4)


A group of cellular and viral oncogenes including the plt gene of polyoma virus (large T protein), the E1A genes of adenoviruses and rearranged forms of the c-myc oncogene cooperate with oncogenes of a second class, including the cellular ras oncogenes and the pmt gene of polyoma virus in the oncogenic transformation fat embryo fibroblasts (1). The myc, plt and E1A genes induce by themselves an early stage of transformation (“immortalization”). The properties of cells at this stage are of interest, since they may constitute a useful experimental model for the study of a very early stage of tumor progression. Transfer of the genes did not result in the immediate appearance of a tumorigenic potential in vivo, and, in fact most of the properties of cells grown in vitroremained similar to those of the normal controls. In primary rat embryo fibroblast cultures, the only phenotypes consistently associated with the expression of these genes in cell culture were a change in the hormonal growth, indicated by a decrease in their requirement in serum factors, and the ability of long term growth (2). When rearranged myc genes were transferred into cells of an established line (FR3T3) together with the neor drug-resistance gene, selection in G418 medium produced cell lines which, upon successive generations in culture, exhibited a characteristic high frequency of spontaneous transformation and acquisition of a tumorigenic potential in syngeneic animals. Fluctuation assays indicated a wide distribution of frequencies between parallel sub-cultures, indicative of the random occurrence of secondary genetic events leading to tumorigenesis (3).


Viral Oncogene Tumorigenic Potential Polyoma Virus Random Occurrence Established Line 
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.


  1. (1).
    Cuzin, F., 1984, Biochim. Biophys. Acta, 781: 193–204.Google Scholar
  2. (2).
    Rassoulzadegan, M. et al., 1983, Proc. Natl. Acad. Sci. USA, 80:4354–4358. Mougneau, E. et al., 1984, Proc. Natl. Acad. Sci. USA 81: 5758–5762.Google Scholar
  3. (3).
    Mougneau, E., Cerni, C. and Cuzin F., manuscript in preparation.Google Scholar
  4. (4).
    Connan, G. et al., 1985, Nature 314: 277–279.PubMedCrossRefGoogle Scholar
  5. (5).
    Cerni, C. et al., 1986, Exp. Cell Res., in press.Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1987

Authors and Affiliations

  • Evelyne Mougneau
    • 1
  • Christa Cerni
    • 2
  • Francois Cuzin
    • 1
  1. 1.Unité 273 der I’INSERMUniversité de NiceFrance
  2. 2.lnstitute for Tumor BiologyUniversity of ViennaAustria

Personalised recommendations