ArticleOncogene2010
p53 suppresses structural chromosome instability after mitotic arrest in human cells.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- The role of clonal progression leading to the development of therapy-related myeloid neoplasms.Annals of hematology · 2024Pooled it
- Correlative Analysis of Genetic Alterations and Everolimus Benefit in Hormone Receptor-Positive, Human Epidermal Growth Factor Receptor 2-Negative Advanced Breast Cancer: Results From BOLERO-2.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2016Trial
- Targeting programmed cell death: a novel therapeutic paradigm for cancer based on mode-of-death classification.Apoptosis : an international journal on programmed cell death · 2026Review
- Allelic Imbalance and Chromothripsis Lead to Diversity in Japanese Tumor Genomes With Whole-Genome Duplication.Cancer science · 2025Article
- The Role of p53 Mutations in Early and Late Response to Mitotic Aberrations.Biomolecules · 2025Review
- Article
- Mutational spectrum of breast cancer by shallow whole-genome sequencing of cfDNA and tumor gene panel analysis.PloS one · 2024Article
- Article
- Permission to pass: on the role of p53 as a gatekeeper for aneuploidy.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023Review
- Smoking-associated Downregulation of FILIP1L Enhances Lung Adenocarcinoma Progression Through Mucin Production, Inflammation, and Fibrosis.Cancer research communications · 2022Article
- FILIP1L Loss Is a Driver of Aggressive Mucinous Colorectal Adenocarcinoma and Mediates Cytokinesis Defects through PFDN1.Cancer research · 2021Article
- Chromosomal Instability in Acute Myeloid Leukemia.Cancers · 2021Review
- Genomic and prognostic heterogeneity among RAS/BRAFMolecular oncology · 2021Article
- hCINAP regulates the DNA-damage response and mediates the resistance of acute myelocytic leukemia cells to therapy.Nature communications · 2019Article
- Integrated Analysis of TP53 Gene and Pathway Alterations in The Cancer Genome Atlas.Cell reports · 2019Article
- The responses of cancer cells to PLK1 inhibitors reveal a novel protective role for p53 in maintaining centrosome separation.Scientific reports · 2017Article
- Stable aneuploid tumors cells are more sensitive to TTK inhibition than chromosomally unstable cell lines.Oncotarget · 2017Article
- Mitotic Catastrophe in BC3H1 Cells following Yessotoxin Exposure.Frontiers in cell and developmental biology · 2017Article
- An association between nuclear morphology and immunohistochemical expression of p53 and p16INK4A in lung cancer cells.Medical molecular morphology · 2014Article
- p53-independent effects of Mdm2.Sub-cellular biochemistry · 2014Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The p53 tumor suppressor inhibits the proliferation of cells that undergo prolonged activation of the mitotic checkpoint. However, the function of this antiproliferative response is not well defined. Here, we report that p53 suppresses structural chromosome instability after mitotic arrest in human cells. In both HCT116 colon cancer cells and normal human fibroblasts, DNA breaks occurred during mitotic arrest in a p53-independent manner, but p53 was required to suppress the proliferation and structural chromosome instability of the resulting polyploid cells. In contrast, cells made polyploid without mitotic arrest exhibited neither significant structural chromosome instability nor p53-dependent cell cycle arrest. We also observed that p53 suppressed both the frequency and structural chromosome instability of spontaneous polyploids in HCT116 cells. Furthermore, time-lapse videomicroscopy revealed that polyploidization of p53(-/-) HCT116 cells is frequently accompanied by mitotic arrest. These data suggest that a function of the p53-dependent postmitotic response is the prevention of structural chromosome instability after prolonged activation of the mitotic checkpoint. Accordingly, our study suggests a novel mechanism of tumor suppression for p53, as well as a potential function for p53 in the outcome of antimitotic chemotherapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.