par Telerman, Adam 
;Tuynder, Marcel;Dupressoir, Th.;Robaye, Bernard ;Sigaux, F;Shaulian, E;Oren, M;Rommelaere, Jean ;Amson, Robert
Référence Proceedings of the National Academy of Sciences of the United States of America, 90, 18, page (8702-8706)
Publication Publié, 1993-09
;Tuynder, Marcel;Dupressoir, Th.;Robaye, Bernard ;Sigaux, F;Shaulian, E;Oren, M;Rommelaere, Jean ;Amson, Robert Référence Proceedings of the National Academy of Sciences of the United States of America, 90, 18, page (8702-8706)
Publication Publié, 1993-09
Article révisé par les pairs
| Résumé : | 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. |
