ReviewGenes2019
Type II DNA Topoisomerases Cause Spontaneous Double-Strand Breaks in Genomic DNA.
Review in Genes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 82 citations in OpenAlex.
- DEPACE-seq enables high-fidelity, single-nucleotide-resolution mapping of abasic sites and characterization of dynamic and long-lived AP landscapes in mammalian genomes.Nucleic acids research · 2026Article
- Deletion of TOP2B promoter using CRISPR-Cas9 induces senescence in HEK 293T cells.Biochemistry and biophysics reports · 2026Article
- The landscape of structural variation in pediatric cancer.Cancer cell · 2026Article
- DNA topological regulation in RNA polymerase II transcription.Cellular & molecular biology letters · 2026Review
- CHK1 inhibition increases the therapeutic response to radiotherapy via antitumor immunity in ARID1A-deficient colorectal cancer.Cell death & disease · 2025Article
- Weighted Gene Co-expression Network Analysis and Machine Learning Validation for Identifying Major Genes Related to Sjogren's Syndrome.Biochemical genetics · 2025Article
- Application of Biological Modifiers to a Multiplexed, Human Cell-Based DNA Damage Assay Provides Mechanistic Information on Genotoxicity and Molecular Targets.Environmental and molecular mutagenesis · 2025Article
- The landscape of structural variation in pediatric cancer.bioRxiv : the preprint server for biology · 2025Article
- Evaluation of the Effect of Dibornol on the Level of DNA Damage in the DNA Comet Test In Vivo.Bulletin of experimental biology and medicine · 2024Article
- Identification of key genes associated with cervical cancer based on bioinformatics analysis.BMC cancer · 2024Article
- TDP2 is a regulator of estrogen-responsive oncogene expression.NAR cancer · 2024Article
- Tyrosyl-DNA phosphodiesterase 2 (Tdp2) repairs DNA-protein crosslinks and protects against double strand breaksFrontiers in cell and developmental biology · 2024Article
- XPF interacts with TOP2B for R-loop processing and DNA looping on actively transcribed genes.Science advances · 2023Article
- Targeting and Monitoring Acute Myeloid Leukaemia with Nucleophosmin-1 (International journal of molecular sciences · 2023Review
- ATM suppresses c-Myc overexpression in the mammary epithelium in response to estrogen.Cell reports · 2023Article
- Lestaurtinib induces DNA damage that is related to estrogen receptor activation.Current research in toxicology · 2023Article
- A high-throughput 384-well CometChip platform reveals a role for 3-methyladenine in the cellular response to etoposide-induced DNA damage.NAR genomics and bioinformatics · 2022Article
- Saffron, Its Active Components, and Their Association with DNA and Histone Modification: A Narrative Review of Current Knowledge.Nutrients · 2022Review
- DNA damage to β cells in culture recapitulates features of senescent β cells that accumulate in type 1 diabetes.Molecular metabolism · 2022Article
- Cross-species incompatibility between a DNA satellite and the Drosophila Spartan homolog poisons germline genome integrity.Current biology : CB · 2022Article
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 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type II DNA topoisomerase enzymes (TOP2) catalyze topological changes by strand passage reactions. They involve passing one intact double stranded DNA duplex through a transient enzyme-bridged break in another (gated helix) followed by ligation of the break by TOP2. A TOP2 poison, etoposide blocks TOP2 catalysis at the ligation step of the enzyme-bridged break, increasing the number of stable TOP2 cleavage complexes (TOP2ccs). Remarkably, such pathological TOP2ccs are formed during the normal cell cycle as well as in postmitotic cells. Thus, this 'abortive catalysis' can be a major source of spontaneously arising DNA double-strand breaks (DSBs). TOP2-mediated DSBs are also formed upon stimulation with physiological concentrations of androgens and estrogens. The frequent occurrence of TOP2-mediated DSBs was previously not appreciated because they are efficiently repaired. This repair is performed in collaboration with BRCA1, BRCA2, MRE11 nuclease, and tyrosyl-DNA phosphodiesterase 2 (TDP2) with nonhomologous end joining (NHEJ) factors. This review first discusses spontaneously arising DSBs caused by the abortive catalysis of TOP2 and then summarizes proteins involved in repairing stalled TOP2ccs and discusses the genotoxicity of the sex hormones.
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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.