The DOI matches its Crossref record; 70 of the 70 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“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]
In the citing paper
“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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Genetic instabilities in human cancers
Lengauer, C., Kinzler, K. W., & Vogelstein, B. (1998) · Nature · doi:10.1038/25292 · Cited by 4,168 · cited 5×
“There are four types of genomic instability (IN): subtle sequence instabilities at the nucleotide (NIN) and mismatch (MIN) level, chromosomal instability (CIN), and amplification instability (AIN) [Lengauer et al., 1998].”
BackgroundInfluentialHingorani, S. R., Wang, L., Multani, A. S., Combs, C., Deramaudt, T. B., Hruban, R. H., Rustgi, A. K., Chang, S., & Tuveson, D. A. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.04.023 · Cited by 2,609
Distant metastasis occurs late during the genetic evolution of pancreatic cancer
Yachida, S., Jones, S., Bozic, I., Antal, T., Leary, R., Fu, B., Kamiyama, M., Hruban, R. H., Eshleman, J. R., Nowak, M. A., et al. (2010) · Nature · doi:10.1038/nature09515 · Cited by 2,502
Kaghad, M., Bonnet, H., Yang, A., Créancier, L., Biscan, J.-C., Valent, A., Minty, A. J., Chalon, P., Lélias, J.-M., Dumont, X., et al. (1997) · Cell · doi:10.1016/s0092-8674(00)80540-1 · Cited by 1,659
Altered cell cycle arrest and gene amplification potential accompany loss of wild-type p53
Livingstone, L. R., White, A., Sprouse, J., Livanos, E., Jacks, T., & Tlsty, T. D. (1992) · Cell · doi:10.1016/0092-8674(92)90243-6 · Cited by 1,328
The patterns and dynamics of genomic instability in metastatic pancreatic cancer
Campbell, P. J., Yachida, S., Mudie, L. J., Stephens, P. J., Pleasance, E. D., Stebbings, L. A., Morsberger, L. A., Latimer, C., McLaren, S., Lin, M.-L., et al. (2010) · Nature · doi:10.1038/nature09460 · Cited by 1,317
Mutant p53 gain of function in two mouse models of Li-Fraumeni syndrome
Olive, K. P., Tuveson, D. A., Ruhe, Z. C., Yin, B., Willis, N. A., Bronson, R. T., Crowley, D., & Jacks, T. (2004) · Cell · doi:10.1016/j.cell.2004.11.004 · Cited by 1,308
Takata, M., Sasaki, M. S., Sonoda, E., Morrison, C., Hashimoto, M., Utsumi, H., Yamaguchi‐Iwai, Y., Shinohara, A., & Takeda, S. (1998) · The EMBO Journal · doi:10.1093/emboj/17.18.5497 · Cited by 1,229
Sensing and repairing DNA double-strand breaks
Jackson, S. P. (2002) · Carcinogenesis · doi:10.1093/carcin/23.5.687 · Cited by 1,149
When mutants gain new powers: News from the mutant p53 field
Brosh, R., & Rotter, V. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2693 · Cited by 1,132
Cited by
Sorted by citations
Targeting p53 pathways: mechanisms, structures, and advances in therapy
Wang, H., Guo, M., Wei, H., & Chen, Y. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01347-1 · Cited by 1,016
p53 inhibits CRISPR–Cas9 engineering in human pluripotent stem cells
Ihry, R. J., Worringer, K. A., Salick, M. R., Frias, E., Ho, D., Theriault, K., Kommineni, S., Chen, J., Sondey, M., Ye, C., et al. (2018) · Nature Medicine · doi:10.1038/s41591-018-0050-6 · Cited by 978
The genomic landscape of hypodiploid acute lymphoblastic leukemia
Holmfeldt, L., Wei, L., Díaz-Flores, E., Walsh, M. F., Zhang, J., Ding, L., Payne-Turner, D., Churchman, M. L., Andersson, A., Chen, S.-C., et al. (2013) · Nature Genetics · doi:10.1038/ng.2532 · Cited by 738
Integrated Analysis of TP53 Gene and Pathway Alterations in The Cancer Genome Atlas
Donehower, L. A., Soussi, T., Korkut, A., Liu, Y., Schultz, A., Cardenas, M., Li, X., Babur, Ö., Hsu, T., Lichtarge, O., et al. (2019) · Cell Reports · doi:10.1016/j.celrep.2019.07.001 · Cited by 724
Metastasis as an evolutionary process
Turajlic, S., & Swanton, C. (2016) · Science · doi:10.1126/science.aaf2784 · Cited by 661
Metadata
- 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
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 ›
Are you an author, or do you see a problem with this page? Request a review
