A model for tumor suppression using H-1 parvovirus

Adam Telerman*, Marcel Tuynder, Thierry Dupressoir, Bernard Robaye, François Sigaux, Eitan Shaulian, Moshe Oren, Jean Rommelaere, Robert Amson

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

85 Scopus citations


A model system is proposed to investigate, at the molecular level, the pathways of tumor suppression. As a tool for the selection of cells with a suppressed phenotype, we used the H-1 parvovirus that preferentially kills various neoplastic cells. From the human K562 leukemia cells, we isolated a clone, KS, that is resistant to the cytopathic effect of the H-1 virus and displays a suppressed malignant phenotype. The suppressed malignancy and the cellular resistance to H-1 killing appear to depend on the activity of wild-type p53. Whereas the KS cells express wild-type p53, the protein is undetectable in the parental K562 cells. Experiments with p53 mutants suggest that wild-type p53, in its functionally intact state, contributes to the resistance against the cytopathic effect of H-1 parvovirus.

Original languageAmerican English
Pages (from-to)8702-8706
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number18
StatePublished - 15 Sep 1993
Externally publishedYes


  • Cancer genetics
  • Oncogenes
  • Tumor suppressor genes
  • p53


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