Links between mutant p53 and genomic instability
Open accessAbstract
The tumor suppressor p53 has long been known to play a central role in maintaining a stable genome in the face of toxic insults through its role in promoting cell‐cycle checkpoints, DNA repair, and apoptosis. However, p53 null cells still retain some function of certain checkpoint and repair processes, reducing the genomic changes that otherwise would occur if these mechanisms were absent. Accumulating evidence suggests that mutant forms of p53 proteins may drastically perturb these residual genome‐stabilizing mechanisms through gain‐of‐function interactions with multiple proteins leading to a higher level of genomic instability than in p53 null cells. This review summarizes the current body of evidence that mutp53 plays a role in promoting various forms of genomic instability and provides an overview of current mechanistic proposals. J. Cell. Biochem. 113: 433–439, 2012. © 2011 Wiley Periodicals, Inc.
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Loss of TP53 and RB1 likely occurs early in osteosarcoma transformation, with TP53 inactivation required to propagate abnormal genomes, followed by rapid accumulation of driver lesions such as MYC amplification, PTEN loss and deletion of ATRX.
“Using these genomic aberrations to infer the evolution of the tumours, loss of TP53 and RB1 likely occurs early in the transformation process (with TP53 inactivation required to propagate abnormal genomes 39,40,41 ), followed by rapid accumulation of driver lesions such as MYC amplification, PTEN loss 42 and deletion of ATRX”
From Osteosarcoma (2022) · cites this paper as [41]
The most likely order of events for osteosarcoma evolution is loss of TP53 and RB1 as early events, with TP53 loss likely initiating genomic instability, followed by whole-genome doubling, gain of 8q (CMYC) and loss of 10q (PTEN).
“The most likely order of events for osteosarcoma evolution is loss of TP53 and RB1 as early events, of which TP53 loss is likely the initiator of genomic instability 39,40,41 followed by whole-genome doubling, gain of 8q (CMYC) and loss of 10q (PTEN) 42 .”
From Osteosarcoma (2022) · cites this paper as [41]
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- Authors
- Hanel, W., & Moll, U. M.
- Affiliations
- Stony Brook University (US)
- Corresponding author
- Moll, Ute M.
- Venue
- Journal of Cellular Biochemistry
- Publisher
- Wiley
- Published
- 2012-01-05
- Volume
- 113
- Issue
- 2
- Pages
- 433-439
- ISSN
- 0730-2312 (ISSN-L)
- 1097-4644
- PMC
- PMC4407809
- OpenAlex
- W1984372257
- Cited by
- 216
- References
- 70
- Citations by year
- 2026: 15 · 2025: 7 · 2024: 14 · 2023: 15 · 2022: 22 · 2021: 12 · 2020: 17 · 2019: 18 · 2018: 22 · 2017: 10 · 2016: 16 · 2015: 14 · 2014: 17 · 2013: 10 · 2012: 7
- FWCI
- 1.00
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Cellular Biochemistry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R01CA060664)
- National Institute of General Medical Sciences (T32GM008444)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- mutant p53, gain-of-function p53, genomic instability, p53 tumor suppressor, cell cycle checkpoints, DNA repair, apoptosis, p53-null cells
- MeSH terms
- Aneuploidy, Animals, Cell Survival, DNA Damage, Gene Amplification, Humans, Mutation, Neoplasms, Translocation, Genetic, Tumor Suppressor Protein p53, Genomic Instability
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