The DOI matches its Crossref record; 57 of the 64 references it cites were found in a registry or an index.
Mutant p53 Gain of Function in Two Mouse Models of Li-Fraumeni Syndrome
Open accessAbstract
The p53 tumor suppressor gene is commonly altered in human tumors, predominantly through missense mutations that result in accumulation of mutant p53 protein. These mutations may confer dominant-negative or gain-of-function properties to p53. To ascertain the physiological effects of p53 point mutation, the structural mutant p53R172H and the contact mutant p53R270H (codons 175 and 273 in humans) were engineered into the endogenous p53 locus in mice. p53R270H/+ and p53R172H/+ mice are models of Li-Fraumeni Syndrome; they developed allele-specific tumor spectra distinct from p53+/- mice. In addition, p53R270H/- and p53R172H/- mice developed novel tumors compared to p53-/- mice, including a variety of carcinomas and more frequent endothelial tumors. Dominant effects that varied by allele and function were observed in primary cells derived from p53R270H/+ and p53R172H/+ mice. These results demonstrate that point mutant p53 alleles expressed under physiological control have enhanced oncogenic potential beyond the simple loss of p53 function.
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“Trp53tm2Tyj (ref. 88), Commd10Tg(Vav1-icre)A2Kio (ref. 89; Jackson Laboratory, 008610) and Tg(Tal1-cre/ERT)42-056Jrg (ref. 90) have been previously described.”
From Single-cell multi-omics identifies chronic inflammation as a driver of TP53-mutant leukemic evolution (2023) · cites this paper as [88]
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“Mutant p53-heterozygous mice develop many metastatic tumors that are rare in mice lacking p53 (Lang, et al., 2004; Olive, et al., 2004).”
From The Mdm network and its regulation of p53 activities: a rheostat of cancer risk (2014) · cites this paper as Olive, et al., 2004
Citations
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7 of the 64 references couldn’t be matched to a known paper.
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Repertoires of Autophagy in the Pathogenesis of Ocular Diseases
Li, Y., Jiang, Q. L., Cao, G.-F., Yao, J., & Yan, B. (2015) · Cellular Physiology and Biochemistry · doi:10.1159/000373980 · Cited by 16,351
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TP53 mutations in human cancers: origins, consequences, and clinical use.
Olivier, M., Hollstein, M., & Hainaut, P. (2010) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a001008 · Cited by 2,199
Vousden, K. H., & Lane, D. P. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2147 · Cited by 2,351
Metadata
- Authors
- Olive, K. P., Tuveson, D. A., Ruhe, Z. C., Yin, B., Willis, N. A., Bronson, R. T., Crowley, D., & Jacks, T.
- Affiliations
- Massachusetts Institute of Technology (US)
- Abramson Cancer Center (US)
- Tufts University (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Jacks, Tyler
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2004-12
- Volume
- 119
- Issue
- 6
- Pages
- 847-860
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2079852484
- Cited by
- 1,308
- References
- 64
- Citations by year
- 2026: 26 · 2025: 49 · 2024: 52 · 2023: 87 · 2022: 52 · 2021: 64 · 2020: 67 · 2019: 69 · 2018: 74 · 2017: 69 · 2016: 78 · 2015: 75 · 2014: 97 · 2013: 64 · 2012: 51
- FWCI
- 21.50
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- p53, Li-Fraumeni syndrome, gain-of-function mutations, missense mutations, dominant-negative p53, tumor suppressor, mouse model, endothelial tumors, carcinoma, oncogenicity
- MeSH terms
- Alleles, Animals, Carcinoma, Mice, Transgenic, Mutation, Neoplasms, T-Lymphocytes, Gene Expression Regulation, Neoplastic, Genes, p53, Li-Fraumeni Syndrome, Apoptosis, Mice
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