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

doi:10.1073/pnas.90.18.8702

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 journal › Article › peer-review

82 Scopus citations

Abstract

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 language	American English
Pages (from-to)	8702-8706
Number of pages	5
Journal	Proceedings of the National Academy of Sciences of the United States of America
Volume	90
Issue number	18
DOIs	https://doi.org/10.1073/pnas.90.18.8702
State	Published - 15 Sep 1993
Externally published	Yes

Keywords

Cancer genetics
Oncogenes
Tumor suppressor genes
p53

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1073/pnas.90.18.8702

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title = "A model for tumor suppression using H-1 parvovirus",

abstract = "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.",

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AU - Tuynder, Marcel

AU - Dupressoir, Thierry

AU - Robaye, Bernard

AU - Sigaux, François

AU - Shaulian, Eitan

AU - Oren, Moshe

AU - Rommelaere, Jean

AU - Amson, Robert

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AB - 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.

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A model for tumor suppression using H-1 parvovirus

Abstract

Keywords

UN SDGs

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