ReviewOncogene2002
Loss of p53 and centrosome hyperamplification.
Review in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
82 citing papers in PubMed, 185 citations in OpenAlex.
- Sensing centrosome amplification: the interface between centriole duplication and autophagy.Nature communications · 2026Article
- Review
- Review
- Radiotherapy modulates tumor cell fate decisions: a review.Radiation oncology (London, England) · 2022Review
- CK1 Is a Druggable Regulator of Microtubule Dynamics and Microtubule-Associated Processes.Cancers · 2022Review
- Circulating Tumor Cells in Breast Cancer Patients: A Balancing Act between Stemness, EMT Features and DNA Damage Responses.Cancers · 2022Review
- Keep Calm and Carry on with Extra Centrosomes.Cancers · 2022Review
- Genomic landscape of a mouse model of diffuse-type gastric adenocarcinoma.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2022Article
- Identification of LncRNA Prognostic Signature Associated With Genomic Instability in Pancreatic Adenocarcinoma.Frontiers in oncology · 2022Article
- Centrosome instability: when good centrosomes go bad.Cellular and molecular life sciences : CMLS · 2021Review
- HN1 interacts with γ-tubulin to regulate centrosomes in advanced prostate cancer cells.Cell cycle (Georgetown, Tex.) · 2021Article
- Unraveling pathologies underlying chromosomal instability in cancers.Cancer science · 2021Review
- Tuning SAS-6 architecture with monobodies impairs distinct steps of centriole assembly.Nature communications · 2021Article
- p53 controls genomic stability and temporal differentiation of human neural stem cells and affects neural organization in human brain organoids.Cell death & disease · 2020Article
- IC261, a specific inhibitor of CK1δ/ε, promotes aerobic glycolysis through p53-dependent mechanisms in colon cancer.International journal of biological sciences · 2020Article
- How the Other Half Lives: What p53 Does When It Is Not Being a Transcription Factor.International journal of molecular sciences · 2019Review
- p53 mitotic centrosome localization preserves centrosome integrity and works as sensor for the mitotic surveillance pathway.Cell death & disease · 2019Article
- Review
- Integrated Analysis of TP53 Gene and Pathway Alterations in The Cancer Genome Atlas.Cell reports · 2019Article
- Cytokinesis defects and cancer.Nature reviews. Cancer · 2019Review
22 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Loss or mutational inactivation of p53 has been shown to lead to abnormal amplification of centrosomes through deregulation of the centrosome duplication cycle and failure to undergo cytokinesis. In mouse cells, most cases of centrosome hyperamplification are attributed to deregulation of centrosome duplication. The presence of excess copies of centrosomes increases the frequency of mitotic defects, leading to unbalanced chromosome transmission to daughter cells. p53 controls centrosome duplication via transactivation-dependent and transactivation-independent mechanisms. In its transactivation-dependent control, p21(Waf1/Cip1) acts as a major effector, likely guarding against untimely activation of CDK2/cyclin E kinase, hence ensuring the coordinated initiation of centrosome and DNA duplication. p53 appears to exert its transactivation-independent control through direct physical binding to the centrosomes.
Indexed as
Identifiers
What OpenQuestion holds
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.