ReviewTrends in cancer2017
Mitotic DNA Damage Response: At the Crossroads of Structural and Numerical Cancer Chromosome Instabilities.
Review in Trends in cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 78 citations in OpenAlex.
- USP15 regulates mitotic fidelity, metastatic potential, and chemotherapeutic response in ovarian cancer cells.Molecular therapy. Oncology · 2026Article
- Synthesis and anticancer evaluation of novel thioimidazole derivatives bearing a trimethoxyphenyl moiety.Scientific reports · 2026Article
- Aurora kinase B phosphorylates ZBP1 to drive PANoptosis following treatment with PARP and ATR inhibitors combination.Nature communications · 2025Article
- Chronic sublethal exposure to methylmercury lengthens telomeres in developing zebra finches.Environmental pollution (Barking, Essex : 1987) · 2025Article
- Novel BRCA1-PLK1-CIP2A axis orchestrates homologous recombination-mediated DNA repair to maintain chromosome integrity during oocyte meiosis.Nucleic acids research · 2025Article
- DNA Damage, Telomere and Centromere Dysfunction in Chromothripsis Rearrangements.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Pan-cancer genetic profiles of mitotic DNA integrity checkpoint protein kinases.Cancer biomarkers : section A of Disease markers · 2024Article
- Developmental signals control chromosome segregation fidelity during pluripotency and neurogenesis by modulating replicative stress.Nature communications · 2024Article
- Article
- The two sides of chromosomal instability: drivers and brakes in cancer.Signal transduction and targeted therapy · 2024Review
- Distinct characteristics of the DNA damage response in mammalian oocytes.Experimental & molecular medicine · 2024Review
- ReCorDE: a framework for identifying drug classes targeting shared vulnerabilities with applications to synergistic drug discovery.Frontiers in oncology · 2024Article
- Cold Tumour Phenotype Explained Through Whole Genome Sequencing in Clinical Nasopharyngeal Cancer: A Preliminary Study.ImmunoTargets and therapy · 2024Article
- Vinorelbine Alters lncRNA Expression in Association with EGFR Mutational Status and Potentiates Tumor Progression Depending on NSCLC Cell Lines' Genetic Profile.Biomedicines · 2023Article
- An antioxidant screen identifies ascorbic acid for prevention of light-induced mitotic prolongation in live cell imaging.Communications biology · 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
- Improving Localized Radiotherapy for Glioblastoma via Small Molecule Inhibition of KIF11.Cancers · 2023Article
- The pediatric leukemia oncoprotein NUP98-KDM5A induces genomic instability that may facilitate malignant transformation.Cell death & disease · 2023Article
- Oocytes can repair DNA damage during meiosis via a microtubule-dependent recruitment of CIP2A-MDC1-TOPBP1 complex from spindle pole to chromosomes.Nucleic acids research · 2023Article
- Intrinsic signalling factors associated with cancer cell-cell fusion.Cell communication and signaling : CCS · 2023Review
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 4 institutions in 2 countries.
Funding
Abstract
DNA double-strand breaks (DSBs) prevent cells from entering mitosis allowing cells to repair their genomic damage. Little is known about the response to DSBs once cells have already committed to mitosis. Here, we review the genome-protective role of the mitotic DNA damage response (DDR) and evidence suggesting that its untimely activation induces chromosome segregation errors and paradoxically undermines genomic integrity. In contrast to normal cells, cancer cells coopt this pathway to propagate structural and numerical chromosomal instabilities. Cells derived from genomically unstable tumors exhibit evidence for a partially activated DDR during mitosis, which leads to ongoing chromosome segregation errors. Thus, a thorough understanding of the consequences of mitotic DNA damage is key to our ability to devise novel anticancer therapeutic strategies.
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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.