Cited by 220Cancer-related Molecular PathwaysDNA Repair MechanismsChromatin Remodeling and Cancer

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Links between mutant p53 and genomic instability

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Hanel, Walter, Moll, Ute M.·2012·Journal of Cellular Biochemistry

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Abstract

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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Authors: Hanel, W., & Moll, U. M.
Affiliations: Stony Brook University (US)
Corresponding author: Moll, Ute M.
ORCID: Hanel, Walter
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
DOI: 10.1002/jcb.23400
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
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
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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Links between mutant p53 and genomic instability

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