Cited by 4,649Cancer-related Molecular PathwaysDevelopmental Biology and Gene RegulationCell death mechanisms and regulation

Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours

Donehower, Lawrence A., Harvey, Michele, Slagle, Betty L., McArthur, Mark J., Montgomery, Charles A., Butel, Janet S., Bradley, Allan·1992·Nature

Abstract

Mutations in the p53 tumour-suppressor gene are the most frequently observed genetic lesions in human cancers. To investigate the role of the p53 gene in mammalian development and tumorigenesis, a null mutation was introduced into the gene by homologous recombination in murine embryonic stem cells. Mice homozygous for the null allele appear normal but are prone to the spontaneous development of a variety of neoplasms by 6 months of age. These observations indicate that a normal p53 gene is dispensable for embryonic development, that its absence predisposes the animal to neoplastic disease, and that an oncogenic mutant form of p53 is not obligatory for the genesis of many types of tumours.

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Crossref · 10.1038/356215a0

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1 of 1 references verified0 citation errors · 0 not checkable

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Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • This enhanced muscle function, restoring the Dmd reading frame and enabling potential treatment for Duchenne muscular dystrophy.

    “This enhanced muscle function, restoring the Dmd reading frame and enabling potential treatment for Duchenne muscular dystrophy.”
  • Tabebordbar used adeno-associated viral vectors to deliver CRISPR/Cas9 into an mdx mouse model, deleting the mutated exon 23.

    “For instance, Tabebordbar [13] used adeno-associated viral vectors to deliver CRISPR/Cas9 into an mdx mouse model, deleting the mutated exon 23.”
  • Tp53-knockout mice are born at normal Mendelian ratios and lack apparent phenotypic alterations but are prone to develop spontaneous tumours at around 6 months of age.

    “Tp53 - knockout mice are born at normal Mendelian ratios and lack apparent phenotypic alterations but are prone to develop spontaneous tumours at around 6 months of age 127,128 .”

    From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [127]

  • After inactivation of the TP53 gene in mice, cells lacking functional p53 cannot respond appropriately to external stimuli, resulting in a high probability of tumors.

    “Studies have revealed that after inactivation of the TP53 gene (encoding p53) in mice, cells lacking functional p53 cannot respond appropriately to external stimuli, resulting in a high probability of tumors [7].”
  • Complete loss of Per2 function reduced the average life span of p53−/− mice from 6 months to 4 months.

    “Complete loss of Per2 function reduced the average life span of p53− /− mice from 6 months to 4 months”

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Authors
Donehower, L. A., Harvey, M., Slagle, B. L., McArthur, M. J., Montgomery, C. A., Butel, J. S., & Bradley, A.
Affiliations
Baylor College of Medicine (US)
Venue
Nature
Published
1992-03
Volume
356
Issue
6366
Pages
215-221
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
OpenAlex
W2126679757
Cited by
4,649
References
1
Citations by year
2026: 16 · 2025: 48 · 2024: 51 · 2023: 74 · 2022: 76 · 2021: 80 · 2020: 86 · 2019: 92 · 2018: 84 · 2017: 96 · 2016: 119 · 2015: 89 · 2014: 121 · 2013: 146 · 2012: 157
FWCI
82.13
Type
journal article
Language
en
Open access
closed
Locations
  • Nature (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
p53, tumor suppressor, spontaneous tumors, carcinogenesis, embryonic development, mouse model, neoplasms
MeSH terms
Alleles, Animals, Base Sequence, Blastocyst, DNA, Exons, Female, Genetic Vectors, Heterozygote, Homozygote, Male, Mice, Inbred CBA, Mice, Inbred C57BL, Mice, Transgenic, Molecular Sequence Data, Mutation, Neoplasms, Experimental, RNA, Messenger, Stem Cells, Blotting, Southern, Polymerase Chain Reaction, Genes, p53, Tumor Suppressor Protein p53, Mice

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