ReviewJournal of cellular physiology2016
Mechanisms and Consequences of Double-Strand DNA Break Formation in Chromatin.
Review in Journal of cellular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 268 papers, 2 of them syntheses 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
268 citing papers in PubMed, 2 syntheses or guidelines pooled it, 472 citations in OpenAlex.
- A systematic review of omics discovery studies to identify pertinent metabolic pathways for locally advanced rectal cancer in response to neoadjuvant chemoradiotherapy.Metabolomics : Official journal of the Metabolomic Society · 2025Pooled it
- A Meta-Analysis for Association of XRCC1, XRCC2 and XRCC3 Polymorphisms with Susceptibility to Thyroid Cancer.Asian Pacific journal of cancer prevention : APJCP · 2021Pooled it
- Expanding the therapeutic scope of PARP inhibitors in breast cancer: current indications and future directions.The Journal of clinical investigation · 2026Review
- Synthetic lethality in cancer: mechanisms, therapeutic exploitation and clinical translation.Signal transduction and targeted therapy · 2026Review
- Modulation of DNA Damage by Epstein-Barr Virus (EBV).Viruses · 2026Review
- Impact of Methylparaben on Cumulus Cell DNA Integrity and Porcine Oocyte Developmental Competence In Vitro.Journal of applied toxicology : JAT · 2026Article
- Basic-patch mutations in bacteriophage T4 Rad50 uncouple ATPase activation from processive nuclease activity.Bioscience reports · 2026Article
- Homologous recombination is essential for DNA damage-induced regeneration of Drosophila testis germline stem cells.Development (Cambridge, England) · 2026Article
- Thyroid cancer and double-strand DNA break repair: The potential role of the MRN complex pathogenic variants.Journal of clinical & translational endocrinology · 2026Review
- Article
- Ribonucleotide errors, RNase HII, and ribonucleotide excision repair.Critical reviews in biochemistry and molecular biology · 2026Review
- A targetable FTO/SLC7A11/CBS/CTH axis controls cysteine metabolism, growth and survival in NSCLC.Science advances · 2026Article
- Not just splitting hairs-monitoring environmental chemical exposures, their biological effects and their social determinants with hair shafts and follicles: a narrative review.Environmental health : a global access science source · 2026Review
- Genes shielded, repeats exposed: mutation bias in the midge Chironomus riparius.G3 (Bethesda, Md.) · 2026Article
- Article
- Stiffness-dependent alveolar type II cell senescence in idiopathic pulmonary fibrosis.Cell communication and signaling : CCS · 2026Article
- K63-linked ubiquitylation of S2P-RNAPII regulates transcription in a DNAPK inter-dependent manner in response to double-strand breaks.Nucleic acids research · 2026Article
- Calretinin and Parvalbumin Trapping of TDP43 and XRCC1 Instructs Neocortical Interneuron Death in Neonatal Hypoxic-Ischemic Encephalopathy.Biomolecules · 2026Article
- SFPQ Promotes Homologous Recombination via mRNA Stabilization of RAD51 and Its Paralogs.Journal of molecular biology · 2026Article
- A monofunctional-like mutant of DNA glycosylase NTHL1 changes the dynamics of DNA repair during acute oxidative stress.The Journal of biological chemistry · 2026Article
208 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
All organisms suffer double-strand breaks (DSBs) in their DNA as a result of exposure to ionizing radiation. DSBs can also form when replication forks encounter DNA lesions or repair intermediates. The processing and repair of DSBs can lead to mutations, loss of heterozygosity, and chromosome rearrangements that result in cell death or cancer. The most common pathway used to repair DSBs in metazoans (non-homologous DNA end joining) is more commonly mutagenic than the alternative pathway (homologous recombination mediated repair). Thus, factors that influence the choice of pathways used DSB repair can affect an individual's mutation burden and risk of cancer. This review describes radiological, chemical, and biological mechanisms that generate DSBs, and discusses the impact of such variables as DSB etiology, cell type, cell cycle, and chromatin structure on the yield, distribution, and processing of DSBs. The final section focuses on nucleosome-specific mechanisms that influence DSB production, and the possible relationship between higher order chromosome coiling and chromosome shattering (chromothripsis).
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.