Cited by 1,308Cancer-related Molecular PathwaysChromatin Remodeling and CancerPI3K/AKT/mTOR signaling in cancer

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Mutant p53 Gain of Function in Two Mouse Models of Li-Fraumeni Syndrome

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Olive, Kenneth P., Tuveson, David A., Ruhe, Zachary C., Yin, Bob, Willis, Nicholas A., Bronson, Roderick T., Crowley, Denise, Jacks, Tyler·2004·Cell

DOI 10.1016/j.cell.2004.11.004

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Abstract

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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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: Olive, Kenneth P.
Tuveson, David A.
Ruhe, Zachary C.
Willis, Nicholas A.
Bronson, Roderick T.
Jacks, Tyler
Venue: Cell
Publisher: Elsevier BV
Published: 2004-12
Volume: 119
Issue: 6
Pages: 847-860
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/j.cell.2004.11.004
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: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 3150 d)
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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Mutant p53 Gain of Function in Two Mouse Models of Li-Fraumeni Syndrome

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