ReviewOncogene2004
Cell death by mitotic catastrophe: a molecular definition.
Review in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 523 papers.
What it found
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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.
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Who cites it
523 citing papers in PubMed, 1,234 citations in OpenAlex.
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- CFI-400945 enhances radiosensitivity in colorectal cancer models by promoting mitotic dysregulation and DNA damage-associated apoptosis.Cancer cell international · 2026Article
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- Tissue-specific DNA repair strategies underlie apparent high transposon activity in the Caenorhabditis elegans soma.G3 (Bethesda, Md.) · 2026Article
- ATR and PKMYT1 Inhibition Resensitizes a Subset of TNBC Patient-Derived Models to Carboplatin, Inducing Mitotic Catastrophe.Cancer research communications · 2026Article
- Transient p53/p21 activation selectively protects healthy human hair follicles and their stem cells from chemotherapy.The Journal of clinical investigation · 2026Article
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- HNRNPH1 drives glioblastoma progression by regulating the splicing of cell cycle genes.Cell death & disease · 2026Article
- Emerging Roles of Tubulin Isoforms and Their Post-Translational Modifications in Microtubule-Based Transport and Cellular Functions.Biomolecules · 2026Review
- Cellular responses to targeted radionuclide therapy: rethinking radiobiology under continuous low dose rates.Frontiers in oncology · 2026Review
- The fluoropyrimidine polymer CF10 synergizes with 5-ethynyl-2'-deoxyuridine by promoting telomere attrition and mitotic catastrophe.NAR molecular medicine · 2026Article
- Drosophila melanogaster: an old and future ally to radiobiology.Journal of radiation research · 2025Review
- Molecular profiling of endometrial cancer in Martinique reveals frequent CCNE1 amplification in poor prognosis tumors.Scientific reports · 2025Article
- Pre-rRNAs control mitosis by maintaining chromosomal segregation through protecting SMC2 from AURKA-mediated phosphorylation.Cell death & disease · 2025Article
- Pan-cancer Myc modulator that targets Myc-α-tubulin interaction to drive selective mitotic catastrophe.Scientific reports · 2025Article
- Primary cilium disappearance in podocytes during vertebrate phylogeny revealed by array tomography.Cell and tissue research · 2025Article
- Distinct evolutionary trajectories of subgenomic centromeres in polyploid wheat.Genome biology · 2025Article
463 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
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The current literature is devoid of a clearcut definition of mitotic catastrophe, a type of cell death that occurs during mitosis. Here, we propose that mitotic catastrophe results from a combination of deficient cell-cycle checkpoints (in particular the DNA structure checkpoints and the spindle assembly checkpoint) and cellular damage. Failure to arrest the cell cycle before or at mitosis triggers an attempt of aberrant chromosome segregation, which culminates in the activation of the apoptotic default pathway and cellular demise. Cell death occurring during the metaphase/anaphase transition is characterized by the activation of caspase-2 (which can be activated in response to DNA damage) and/or mitochondrial membrane permeabilization with the release of cell death effectors such as apoptosis-inducing factor and the caspase-9 and-3 activator cytochrome c. Although the morphological aspect of apoptosis may be incomplete, these alterations constitute the biochemical hallmarks of apoptosis. Cells that fail to execute an apoptotic program in response to mitotic failure are likely to divide asymmetrically in the next round of cell division, with the consequent generation of aneuploid cells. This implies that disabling of the apoptotic program may actually favor chromosomal instability, through the suppression of mitotic catastrophe. Mitotic catastrophe thus may be conceived as a molecular device that prevents aneuploidization, which may participate in oncogenesis. Mitotic catastrophe is controlled by numerous molecular players, in particular, cell-cycle-specific kinases (such as the cyclin B1-dependent kinase Cdk1, polo-like kinases and Aurora kinases), cell-cycle checkpoint proteins, survivin, p53, caspases and members of the Bcl-2 family.
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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.