ArticleCancer discovery2014
DNA-damage response during mitosis induces whole-chromosome missegregation.
Article in Cancer discovery, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.
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
95 citing papers in PubMed, 1 synthesis or guideline pooled it, 157 citations in OpenAlex.
- Rare variants in BRCA2 and CHEK2 are associated with the risk of urinary tract cancers.Scientific reports · 2016Pooled it
- Chromosomal instability in cancer: sources, consequences and new therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- Genome near-haploidization in CDC73-wildtype parathyroid tumors.Scientific reports · 2026Article
- Article
- Aurora kinase B phosphorylates ZBP1 to drive PANoptosis following treatment with PARP and ATR inhibitors combination.Nature communications · 2025Article
- An Aurora kinase A-BOD1L1-PP2A B56 axis promotes chromosome segregation fidelity.Cell reports · 2025Article
- The Role of p53 Mutations in Early and Late Response to Mitotic Aberrations.Biomolecules · 2025Review
- Cell cycle proteins: Linking the cell cycle to tumors.Oncology research · 2025Review
- Chk2 sustains PLK1 activity in mitosis to ensure proper chromosome segregation.Nature communications · 2024Article
- Base Excision Repair in Mitotic Cells and the Role of Apurinic/Apyrimidinic Endonuclease 1 (APE1) in Post-Mitotic Transcriptional Reactivation of Genes.International journal of molecular sciences · 2024Article
- TET2 germline variants promote kidney disease by impairing DNA repair and activating cytosolic nucleotide sensors.Nature communications · 2024Article
- Review
- The yin and yang of chromosomal instability in prostate cancer.Nature reviews. Urology · 2024Review
- Article
- An Aurora kinase A-BOD1L1-PP2A B56 Axis promotes chromosome segregation fidelity.bioRxiv : the preprint server for biology · 2024Article
- Boveri and beyond: Chromothripsis and genomic instability from mitotic errors.Molecular cell · 2024Review
- New characterization and safety evaluation of human limbal stem cells used in clinical application: fidelity of mitotic process and mitotic spindle morphologies.Stem cell research & therapy · 2023Article
- Biomaterial-enabled therapeutic modulation of cGAS-STING signaling for enhancing antitumor immunity.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Review
- Chromosomal instability and its effect on cell lines.Cancer reports (Hoboken, N.J.) · 2023Review
- Exploring the ATR-CHK1 pathway in the response of doxorubicin-induced DNA damages in acute lymphoblastic leukemia cells.Cell biology and toxicology · 2023Article
35 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
5 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledMany cancers display both structural (s-CIN) and numerical (w-CIN) chromosomal instabilities. Defective chromosome segregation during mitosis has been shown to cause DNA damage that induces structural rearrangements of chromosomes (s-CIN). In contrast, whether DNA damage can disrupt mitotic processes to generate whole chromosomal instability (w-CIN) is unknown. Here, we show that activation of the DNA-damage response (DDR) during mitosis selectively stabilizes kinetochore-microtubule (k-MT) attachments to chromosomes through Aurora-A and PLK1 kinases, thereby increasing the frequency of lagging chromosomes during anaphase. Inhibition of DDR proteins, ATM or CHK2, abolishes the effect of DNA damage on k-MTs and chromosome segregation, whereas activation of the DDR in the absence of DNA damage is sufficient to induce chromosome segregation errors. Finally, inhibiting the DDR during mitosis in cancer cells with persistent DNA damage suppresses inherent chromosome segregation defects. Thus, the DDR during mitosis inappropriately stabilizes k-MTs, creating a link between s-CIN and w-CIN. SIGNIFICANCE: The genome-protective role of the DDR depends on its ability to delay cell division until damaged DNA can be fully repaired. Here, we show that when DNA damage is induced during mitosis, the DDR unexpectedly induces errors in the segregation of entire chromosomes, thus linking structural and numerical chromosomal instabilities.
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.