ReviewOncogene2013
DNA damage associated with mitosis and cytokinesis failure.
Review in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 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
85 citing papers in PubMed, 169 citations in OpenAlex.
- Dual Inhibition of TRIP13 and Aurora A Induces Mitotic DNA Damage and Concurrent Pyroptotic-Apoptotic Cell Death in Rb-Deficient Cancer Cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- The micronucleus assay in exfoliated buccal cells for occupational exposure studies: an overview.Mutagenesis · 2026Review
- Novel KIF22 Variants Disrupt Mitosis in Human Chondrocytes and Expand SEMDJL2 Mechanisms.bioRxiv : the preprint server for biology · 2026Article
- The fluoropyrimidine polymer CF10 synergizes with 5-ethynyl-2'-deoxyuridine by promoting telomere attrition and mitotic catastrophe.NAR molecular medicine · 2026Article
- Unraveling the triad of hypoxia, cancer cell stemness, and drug resistance.Journal of hematology & oncology · 2025Review
- Pan-cancer genetic profiles of mitotic DNA integrity checkpoint protein kinases.Cancer biomarkers : section A of Disease markers · 2024Article
- Low-Molecular Weight Cyclin E Confers a Vulnerability to PKMYT1 Inhibition in Triple-Negative Breast Cancer.Cancer research · 2024Article
- Inhibition of Aberrantly Overexpressed Polo-like Kinase 4 Is a Potential Effective Treatment for DNA Damage Repair-Deficient Uterine Leiomyosarcoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Eg5 UFMylation promotes spindle organization during mitosis.Cell death & disease · 2024Article
- In vitro evolution and whole genome analysis to study chemotherapy drug resistance in haploid human cells.Scientific reports · 2024Article
- The DNA Damage Response (DDR) landscape of endometrial cancer defines discrete disease subtypes and reveals therapeutic opportunities.NAR cancer · 2024Article
- Primary sex ratio in euploid embryos of consanguine couples after IVF/ICSI.Journal of assisted reproduction and genetics · 2024Article
- Small molecule agents for triple negative breast cancer: Current status and future prospects.Translational oncology · 2024Review
- Optimizing cancer therapy: a review of the multifaceted effects of metronomic chemotherapy.Frontiers in cell and developmental biology · 2024Review
- The Blocking of Drug Resistance Channels by Selected Hydrophobic Statins in Chemoresistance Human Melanoma.Biomolecules · 2023Article
- A robust dual gene ON-OFF toggle directed by two independent promoter-degron pairs.Journal of cell science · 2023Article
- Lymphocyte antigen 6K signaling to aurora kinase promotes advancement of the cell cycle and the growth of cancer cells, which is inhibited by LY6K-NSC243928 interaction.Cancer letters · 2023Article
- Analysis of a rare progeria variant of Barrier-to-autointegration factor in Drosophila connects centromere function to tissue homeostasis.Cellular and molecular life sciences : CMLS · 2023Article
- Whole-Genome Duplication and Genome Instability in Cancer Cells: Double the Trouble.International journal of molecular sciences · 2023Review
- Whole-Genome Doubling as a source of cancer: how, when, where, and why?Frontiers in cell and developmental biology · 2023Review
25 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
Mitosis is a highly dynamic process, aimed at separating identical copies of genomic material into two daughter cells. A failure of the mitotic process generates cells that carry abnormal chromosome numbers. Such cells are predisposed to become tumorigenic upon continuous cell division and thus need to be removed from the population to avoid cancer formation. Cells that fail in mitotic progression indeed activate cell death or cell cycle arrest pathways; however, these mechanisms are not well understood. Growing evidence suggests that the formation of de novo DNA damage during and after mitotic failure is one of the causal factors that initiate those pathways. Here, we analyze several distinct malfunctions during mitosis and cytokinesis that lead to de novo DNA damage generation.
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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.