Spontaneous mutation of cell oncogenes plays a minor role in neoplastic transformation of virus-induced murine T-cell lymphomas

D. Gasparotto, R. Maestro, T. Vukosavljevic, S. Piccinin, A. Sandrin, S. Rizzo, M. Boiocchi

Research output: Contribution to journalArticlepeer-review

Abstract

Mink cell focus-forming viruses (MCF) are slow-transforming retroviruses that are able to accelerate the appearance of T-cell lymphomas when injected in newborn AKR mice. Activation of proto-oncogenes by proviral insertion is thought to be the major mechanism by which these viruses exert their oncogenic potential. However, molecular phenomena not strictly virus-determined, such as mutations in cellular oncogenes/tumor suppressor genes or chromosome aberrations, have been hypothesized to contribute to the achievement of the fully neoplastic phenotype in MCF-infected mice. To evaluate the role of spontaneous mutagenesis phenomena in murine virus-induced lymphomagenesis, we analyzed a series of 18 MCF247-induced thymic lymphomas and derived cell lines for the presence of p53 and c-ras gene mutations. Only 1 mutation at the p53 gene and 1 mutation at the ki-ras gene were detected in our study. Our results suggest that spontaneous mutagenesis plays a minor role in virus-induced lymphomagenesis and support the notion that multiple proviral insertions could be the prevalent mechanism of transformation in this experimental system.

Original languageEnglish
Pages (from-to)268-272
Number of pages5
JournalTumori
Volume81
Issue number4
Publication statusPublished - 1995

Keywords

  • c-ras
  • MCF
  • murine lymphomagenesis
  • p53

ASJC Scopus subject areas

  • Cancer Research

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