ArticleThe Journal of cell biology2018
Centrosome amplification arises before neoplasia and increases upon p53 loss in tumorigenesis.
Article in The Journal of cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 71 citations in OpenAlex.
- Tetraploids or polyploid giants: who is truly dangerous?Trends in cell biology · 2026Review
- CenSegNet: a generalist high-throughput deep learning framework for centrosome phenotyping at spatial and single-cell resolution in heterogeneous tissues.Nature communications · 2026Article
- Article
- Role of PLK4 inhibition in cancer therapy.Cancer metastasis reviews · 2025Review
- Review
- High-throughput electron tomography identifies centriole over-elongation as an early event in plasma cell disorders.Leukemia · 2023Article
- Article
- Centrosome amplification promotes cell invasion via cell-cell contact disruption and Rap-1 activation.Journal of cell science · 2023Article
- 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
- Polo-like kinase 4 (Plk4) potentiates anoikis-resistance of p53KO mammary epithelial cells by inducing a hybrid EMT phenotype.Cell death & disease · 2023Article
- Epigenetic alterations impede epithelial-mesenchymal transition by modulating centrosome amplification and Myc/RAS axis in triple negative breast cancer cells.Scientific reports · 2023Article
- The fate of extra centrosomes in newly formed tetraploid cells: should I stay, or should I go?Frontiers in cell and developmental biology · 2023Review
- Identification of a centrosome-related prognostic signature for breast cancer.Frontiers in oncology · 2023Article
- A high-throughput electron tomography workflow reveals over-elongated centrioles in relapsed/refractory multiple myeloma.Cell reports methods · 2022Article
- Article
- Hypoxia Drives Centrosome Amplification in Cancer Cells via HIF1α-dependent Induction of Polo-Like Kinase 4.Molecular cancer research : MCR · 2022Article
- CK1 Is a Druggable Regulator of Microtubule Dynamics and Microtubule-Associated Processes.Cancers · 2022Review
- An updated view on the centrosome as a cell cycle regulator.Cell division · 2022Review
- Moonlighting at the Poles: Non-Canonical Functions of Centrosomes.Frontiers in cell and developmental biology · 2022Review
- Kinesin Family Member C1 (KIFC1/HSET): A Potential Actionable Biomarker of Early Stage Breast Tumorigenesis and Progression of High-Risk Lesions.Journal of personalized medicine · 2021Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Centrosome abnormalities are a typical hallmark of human cancers. However, the origin and dynamics of such abnormalities in human cancer are not known. In this study, we examined centrosomes in Barrett's esophagus tumorigenesis, a well-characterized multistep pathway of progression, from the premalignant condition to the metastatic disease. This human cancer model allows the study of sequential steps of progression within the same patient and has representative cell lines from all stages of disease. Remarkably, centrosome amplification was detected as early as the premalignant condition and was significantly expanded in dysplasia. It was then present throughout malignant transformation both in adenocarcinoma and metastasis. The early expansion of centrosome amplification correlated with and was dependent on loss of function of the tumor suppressor p53 both through loss of wild-type expression and hotspot mutations. Our work shows that centrosome amplification in human tumorigenesis can occur before transformation, being repressed by p53. These findings suggest centrosome amplification in humans can contribute to tumor initiation and progression.
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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.