The DOI matches its Crossref record; 48 of the 48 references it cites were found in a registry or an index.
Mice deficient for p53 are developmentally normal but susceptible to spontaneous tumours
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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In the citing paper
“This enhanced muscle function, restoring the Dmd reading frame and enabling potential treatment for Duchenne muscular dystrophy.”
From A Review of Research on CRISPR/Cas9 Gene Editing Technology in Disease Treatment (2024) · cites this paper as [13]
In the citing paper
“For instance, Tabebordbar [13] used adeno-associated viral vectors to deliver CRISPR/Cas9 into an mdx mouse model, deleting the mutated exon 23.”
From A Review of Research on CRISPR/Cas9 Gene Editing Technology in Disease Treatment (2024) · cites this paper as [13]
In the citing paper
“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]
In the citing paper
“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].”
From Targeting p53–MDM2 interaction by small-molecule inhibitors: learning from MDM2 inhibitors in clinical trials (2022) · cites this paper as [7]
In the citing paper
“Complete loss of Per2 function reduced the average life span of p53− /− mice from 6 months to 4 months”
From Disrupting Circadian Homeostasis of Sympathetic Signaling Promotes Tumor Development in Mice (2010) · cites this paper as [60]
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Metadata
- 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
- 48
- 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
- Licence
- www.springer.com/tdm (tdm)
- 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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