ArticleCell2010
Persistent telomere damage induces bypass of mitosis and tetraploidy.
Article in Cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 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
180 citing papers in PubMed, 286 citations in OpenAlex.
- Multinucleated Giant Cells in Human Pancreatic Cancer Are a Distinct Macrophage Population Undergoing a DNA Damage Response and Associated with an Aggressive Tumor Microenvironment.Cancer immunology research · 2026Article
- Article
- Lamin B1-dependent regulation of human separase in mitosis.Nucleic acids research · 2026Article
- γH2AX and p53 Immunohistochemistry predict the incidence risk of esophageal squamous precancerous lesions.BMC medicine · 2026Article
- Telomere Crisis Shapes Cancer Evolution.Cold Spring Harbor perspectives in biology · 2026Review
- Breaking barriers in pulmonary health of patients with metabolic diseases: senolytics and beyond.Frontiers in aging · 2026Review
- Three-Dimensional Organization of Telomeres: An Emerging Prognostic Biomarker in Multiple Myeloma.Cells · 2025Review
- DNA damage checkpoints balance a tradeoff between diploid- and polyploid-derived arrest failures.Cell reports · 2025Article
- DNA damage checkpoints balance a tradeoff between diploid- and polyploid-derived arrest failures.bioRxiv : the preprint server for biology · 2025Article
- The Role of p53 Mutations in Early and Late Response to Mitotic Aberrations.Biomolecules · 2025Review
- Polyploidy mitigates the impact of DNA damage while simultaneously bearing its burden.Cell death discovery · 2024Article
- A Fungicide, Fludioxonil, Formed the Polyploid Giant Cancer Cells and Induced Metastasis and Stemness in MDA-MB-231 Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2024Article
- Sustained ERK signaling promotes G2 cell cycle exit and primes cells for whole-genome duplication.Developmental cell · 2024Article
- The yin and yang of chromosomal instability in prostate cancer.Nature reviews. Urology · 2024Review
- Surviving the Storm: The Role of Poly- and Depolyploidization in Tissues and Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- CDK4/6 activity is required during GScience (New York, N.Y.) · 2024Article
- p53 regulates diverse tissue-specific outcomes to endogenous DNA damage in mice.Nature communications · 2024Article
- The antagonistic relationship between apoptosis and polyploidy in development and cancer.Seminars in cell & developmental biology · 2024Review
- Whole-genome doubling is a double-edged sword: the heterogeneous role of whole-genome doubling in various cancer types.BMB reports · 2024Review
- Article
120 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Tetraploidization has been proposed as an intermediate step toward aneuploidy in human cancer but a general mechanism for the induction of tetraploidy during tumorigenesis is lacking. We report that tetraploidization occurs in p53-deficient cells experiencing a prolonged DNA damage signal due to persistent telomere dysfunction. Live-cell imaging revealed that these cells have an extended G2 due to ATM/ATR- and Chk1/Chk2-mediated inhibition of Cdk1/CyclinB and eventually bypass mitosis. Despite their lack of mitosis, the cells showed APC/Cdh1-dependent degradation of the replication inhibitor geminin, followed by accumulation of Cdt1, which is required for origin licensing. Cells then entered a second S phase resulting in whole-genome reduplication and tetraploidy. Upon restoration of telomere protection, these tetraploid cells resumed cell division cycles and proliferated. These observations suggest a general mechanism for the induction of tetraploidization in the early stages of tumorigenesis when telomere dysfunction can result from excessive telomere shortening.
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.