Senescence, aging, and malignant transformation mediated by p53 in mice lacking the Brca1 full-length isoform
Open accessAbstract
Senescence may function as a two-edged sword that brings unexpected consequences to organisms. Here we provide evidence to support this theory by showing that the absence of the Brca1 full-length isoform causes senescence in mutant embryos and cultured cells as well as aging and tumorigenesis in adult mice. Haploid loss of p53 overcame embryonic senescence but failed to prevent the adult mutant mice from prematurely aging, which included decreased life span, reduced body fat deposition, osteoporosis, skin atrophy, and decreased wound healing. We further demonstrate that mutant cells that escaped senescence had undergone clonal selection for faster proliferation and extensive genetic/molecular alterations, including overexpression of cyclin D1 and cyclin A and loss of p53. These observations provide the first in vivo evidence that links cell senescence to aging due to impaired function of Brca1 at the expense of tumorigenesis.
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Mice that express two copies of a hypomorphic Brca1 allele along with only one copy of the gene for p53 (Trp53+/-) survive but show marked progeroid symptoms.
“mice that express two copies of a hypomorphic Brca1 allele along with only one copy of the gene for p53 ( Trp53 +/- ) survive but show marked progeroid symptoms 35”
From The common biology of cancer and ageing (2007) · cites this paper as [35]
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- Authors
- Cao, L., Li, W., Kim, S., Brodie, S. G., & Deng, C.-X.
- Affiliations
- National Institutes of Health (US)
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2003-01-15
- Volume
- 17
- Issue
- 2
- Pages
- 201-213
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC195980
- OpenAlex
- W2087849372
- Cited by
- 293
- References
- 64
- Citations by year
- 2026: 5 · 2025: 4 · 2024: 11 · 2023: 8 · 2022: 6 · 2021: 12 · 2020: 10 · 2019: 9 · 2018: 11 · 2017: 12 · 2016: 16 · 2015: 6 · 2014: 14 · 2013: 20 · 2012: 21
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- cellular senescence, aging, BRCA1, p53, malignant transformation, carcinogenesis, premature aging, clonal selection, cyclin D1, cyclin A, osteoporosis, skin atrophy, wound healing, lifespan, fat deposition, mouse model
- MeSH terms
- Aging, Animals, Female, Haploidy, Male, Mice, Mutant Strains, Neoplasms, Experimental, Phenotype, Genes, p53, Cellular Senescence, BRCA1 Protein, Genes, BRCA1, Aging, Premature, Protein Isoforms, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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