The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
The ATM–p53 pathway suppresses aneuploidy-induced tumorigenesis
Open accessAbstract
The spindle assembly checkpoint (SAC) is essential for proper sister chromatid segregation. Defects in this checkpoint can lead to chromosome missegregation and aneuploidy. An increasing body of evidence suggests that aneuploidy can play a causal role in tumorigenesis. However, mutant mice that are prone to aneuploidy have only mild tumor phenotypes, suggesting that there are limiting factors in the aneuploidy-induced tumorigenesis. Here we provide evidence that p53 is such a limiting factor. We show that aneuploidy activates p53 and that loss of p53 drastically accelerates tumor development in two independent aneuploidy models. The p53 activation depends on the ataxia-telangiectasia mutated (ATM) gene product and increased levels of reactive oxygen species. Thus, the ATM-p53 pathway safeguards not only DNA damage but also aneuploidy.
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“Thus, a post mitotic response which involves activation of the p53 pathway is more likely6162.”
From Mitotic Spindle Disruption by Alternating Electric Fields Leads to Improper Chromosome Segregation and Mitotic Catastrophe in Cancer Cells (2015) · cites this paper as [62]
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Metadata
- Authors
- Li, M., Fang, X., Baker, D. J., Guo, L., Gao, X., Wei, Z., Han, S., van Deursen, J. M., & Zhang, P.
- Affiliations
- Baylor College of Medicine (US)
- Mayo Clinic (US)
- The Mayo Clinic, Rochester, MN 55905
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2010-07-27
- Volume
- 107
- Issue
- 32
- Pages
- 14188-14193
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2922543
- OpenAlex
- W2123618943
- Cited by
- 257
- References
- 31
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 17 · 2023: 14 · 2022: 20 · 2021: 15 · 2020: 10 · 2019: 10 · 2018: 20 · 2017: 21 · 2016: 15 · 2015: 21 · 2014: 16 · 2013: 25 · 2012: 25
- FWCI
- 10.26
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Funders
- National Institutes of Health (5r01ca116097-10)
- National Cancer Institute (CA122623, R01-CA116097, R01CA126828, R01CA122623, CA116097)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Microtubule and mitosis dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- ATM, p53, aneuploidy, spindle assembly checkpoint, chromosome missegregation, sister chromatid segregation, reactive oxygen species, tumor suppression, DNA damage response
- MeSH terms
- Aneuploidy, Animals, DNA Damage, DNA-Binding Proteins, Mice, Transgenic, Neoplasms, Tumor Suppressor Protein p53, Protein Serine-Threonine Kinases, Reactive Oxygen Species, Cell Cycle Proteins, Tumor Suppressor Proteins, Mice, Ataxia Telangiectasia Mutated Proteins
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