Cited by 382Cancer-related Molecular PathwaysDNA Repair MechanismsCell death mechanisms and regulation

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The pathological response to DNA damage does not contribute to p53-mediated tumour suppression

Christophorou, M. A., Ringshausen, I., Finch, A. J., Swigart, L. Brown, Evan, G. I.·2006·Nature

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Abstract

The p53 protein has a highly evolutionarily conserved role in metazoans as 'guardian of the genome', mediating cell-cycle arrest and apoptosis in response to genotoxic injury. In large, long-lived animals with substantial somatic regenerative capacity, such as vertebrates, p53 is an important tumour suppressor--an attribute thought to stem directly from its induction of death or arrest in mutant cells with damaged or unstable genomes. Chemotherapy and radiation exposure both induce widespread p53-dependent DNA damage. This triggers potentially lethal pathologies that are generally deemed an unfortunate but unavoidable consequence of the role p53 has in tumour suppression. Here we show, using a mouse model in which p53 status can be reversibly switched in vivo between functional and inactive states, that the p53-mediated pathological response to whole-body irradiation, a prototypical genotoxic carcinogen, is irrelevant for suppression of radiation-induced lymphoma. In contrast, delaying the restoration of p53 function until the acute radiation response has subsided abrogates all of the radiation-induced pathology yet preserves much of the protection from lymphoma. Such protection is absolutely dependent on p19(ARF)--a tumour suppressor induced not by DNA damage, but by oncogenic disruption of the cell cycle.

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Authors: Christophorou, M. A., Ringshausen, I., Finch, A. J., Swigart, L. B., & Evan, G. I.
Affiliations: University of California, San Francisco (US)
Corresponding author: Evan, G. I.
ORCID: Christophorou, M. A.
Ringshausen, I.
Finch, A. J.
Swigart, L. Brown
Evan, G. I.
Venue: Nature
Publisher: Springer Science and Business Media LLC
Published: 2006-09
Volume: 443
Issue: 7108
Pages: 214-217
ISSN: 0028-0836 (ISSN-L)
1476-4687
DOI: 10.1038/nature05077
OpenAlex: W1970249544
Cited by: 382
References: 30
Citations by year: 2026: 6 · 2025: 2 · 2024: 3 · 2023: 10 · 2022: 6 · 2021: 13 · 2020: 11 · 2019: 8 · 2018: 5 · 2017: 17 · 2016: 19 · 2015: 19 · 2014: 26 · 2013: 24 · 2012: 23
FWCI: 21.50
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature (publishedVersion)
PubMed (publishedVersion)
RePEc: Research Papers in Economics (submittedVersion)
mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
Funders: University of California, San Francisco
National Institute on Aging
National Cancer Institute
Topics: Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords: p53, tumor suppression, DNA damage response, radiation-induced lymphoma, whole-body irradiation, ARF, oncogene activation, cell cycle arrest, apoptosis, lymphomagenesis
MeSH terms: Animals, DNA Damage, Lymphoma, Neoplasms, Radiation-Induced, Tumor Suppressor Protein p53, Cyclin-Dependent Kinase Inhibitor p16, Tumor Suppressor Protein p14ARF, Mice

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The pathological response to DNA damage does not contribute to p53-mediated tumour suppression

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