The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Tumor spectrum analysis in p53-mutant mice
Abstract
Background The p53 tumor suppressor gene is mutated in a large percentage of human malignancies, including tumors of the colon, breast, lung and brain. Individuals who inherit one mutant allele of p53 are susceptible to a wide range of tumor types. The gene encodes a transcriptional regulator that may function in the cellular response to DNA damage. The construction of mouse strains carrying germline mutations of p53 facilitates analysis of the function of p53 in normal cells and tumorigenesis.Results In order to study the effects of p53 mutation in vivo, we have constructed a mouse strain carrying a germline disruption of the gene. This mutation removes approximately 40% of the coding capacity of p53 and completely eliminates synthesis of p53 protein. As observed previously for a different germline mutation of p53, animals homozygous for this p53 deletion mutation are viable but highly predisposed to malignancy. Heterozygous animals also have an increased cancer risk, although the distribution of tumor types in these animals differs from that in homozygous mutants. In most cases, tumorigenesis in heterozygous animals is accompanied by loss of the wild-type p53 allele.Conclusion We reaffirm that p53 function is not required for normal mouse development and conclude that p53 status can strongly influence tumor latency and tissue distribution.
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“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 [128]
In the citing paper
“Mutations in p16 , Rb , ARF and TP53 are frequently found in human cancers, and their tumour-suppressive roles have been confirmed in vivo using genetically modified mouse models [25 -29].”
From The role of cellular senescence and SASP in tumour microenvironment (2023) · cites this paper as [25]
In the citing paper
“Mutations in p16 , Rb , ARF and TP53 are frequently found in human cancers, and their tumour-suppressive roles have been confirmed in vivo using genetically modified mouse models [25 -29].”
From The role of cellular senescence and SASP in tumour microenvironment (2023) · cites this paper as [25]
In the citing paper
“Those tumors that did emerge showed activation of alternative lengthening of telomeres (ALT), mutation of p53 and/or a diminished capacity to achieve a fully malignant state (88,100).”
From Telomeres and telomerase in cancer (2010) · cites this paper as [100]
Citations
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Self-citationThe transcription factor Myc controls metabolic reprogramming upon T lymphocyte activation
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“Animals Hif1a and p53-null mice on the C57BL/6 background were purchased from the Jackson Laboratory (Jacks et al., 1994; Ryan et al., 2000) and Hif1a mice were crossed with ROSA26CreERT2 (de Luca et al.”
Method
Metadata
- Authors
- Jacks, T., Remington, L., Williams, B. O., Schmitt, E. M., Halachmi, S., Bronson, R. T., & Weinberg, R. A.
- Affiliations
- Massachusetts Institute of Technology (US)
- Tufts University (US)
- Whitehead Institute for Biomedical Research (US)
- Corresponding author
- Jacks, Tyler
- Venue
- Current Biology
- Publisher
- Elsevier BV
- Published
- 1994-01
- Volume
- 4
- Issue
- 1
- Pages
- 1-7
- ISSN
- 0960-9822 (ISSN-L)
- OpenAlex
- W2088740611
- Cited by
- 2,051
- References
- 5
- Citations by year
- 2026: 17 · 2025: 33 · 2024: 51 · 2023: 46 · 2022: 35 · 2021: 58 · 2020: 63 · 2019: 44 · 2018: 61 · 2017: 57 · 2016: 66 · 2015: 51 · 2014: 75 · 2013: 72 · 2012: 102
- FWCI
- 17.41
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Biology (publishedVersion)
- PubMed (publishedVersion)
- The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
- Funders
- National Institutes of Health (5r35ca039826-10)
- National Cancer Institute (5R35 CA39826)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- p53, tumor suppressor, germline mutations, p53 knockout mice, tumor spectrum, tumor latency, heterozygous carriers, cancer susceptibility, DNA damage response, transcriptional regulation
- MeSH terms
- Alleles, Animals, Base Sequence, Chimera, Chromosome Deletion, Crosses, Genetic, DNA Damage, Female, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Molecular Sequence Data, Neoplasms, Experimental, Polymerase Chain Reaction, Genes, p53, Tumor Suppressor Protein p53, Li-Fraumeni Syndrome, Sequence Deletion, DNA Primers, Mice
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