ReviewCells2020
The Chromatin Response to Double-Strand DNA Breaks and Their Repair.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 72 citations in OpenAlex.
- Unraveling the role of deuterium in cancer: mechanisms, detection techniques, and therapeutic potential.Molecular diversity · 2026Review
- Narciclasine Exerts Anticancer Activity in Colorectal Cancer Cells in Association with HELLS Downregulation and DNA Damage-Associated Responses.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Cell-cycle-dependent regulation of DNA end resection by PLK1 and PLK3 without CtIP level modulation.iScience · 2026Article
- CDW19S coordinates phasic end processing via distinct enzymatic activities.Nucleic acids research · 2026Article
- Article
- Gadd45α silencing alleviates cerebral ischemia-reperfusion injury by suppressing FOXO1 signaling.Scientific reports · 2026Article
- Real-Time Visualization of G2L4 Reverse Transcriptase in DNA Repair via Microhomology-Mediated End Joining.bioRxiv : the preprint server for biology · 2026Article
- Dual-single-guide RNA strategy improves CRISPR-mediated homology-directed repair in Aspergillus.Nucleic acids research · 2026Article
- Inhibiting macrophage-derived lactate transport restores cGAS-STING signalling and enhances antitumour immunity in glioblastoma.Nature cell biology · 2026Article
- Multicolor Laser Scanning Confocal Immunofluorescence Microscopy of DNA Damage Response Biomarkers.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Regulation of drug resistance in bladder urothelial carcinoma by tumor aerobic glycolysis.Journal of translational medicine · 2025Review
- The Role of Transient Crosslinks in the Chromatin Search Response to DNA Damage.International journal of molecular sciences · 2025Article
- DNA shape and epigenomics distinguish the mechanistic origin of human genomic structural variations.Nucleic acids research · 2025Article
- Prominent fibroblast growth factor 21 with less abundant tumor-associated macrophages in hepatic mass of the conditional mgmt-deleted mice using LysM-Cre system.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Cancer Vulnerabilities Through Targeting the ATR/Chk1 and ATM/Chk2 Axes in the Context of DNA Damage.Cells · 2025Review
- Molecular mechanisms of extrachromosomal circular DNA formation.Nucleic acids research · 2025Review
- Diffusion of activated ATM explains γH2AX and MDC1 spread beyond the DNA damage site.iScience · 2024Article
- Chromatin dynamics and RNA metabolism are double-edged swords for the maintenance of plant genome integrity.Nature plants · 2024Review
- The impact of developmental stage, tissue type, and sex on DNA double-strand break repair in Drosophila melanogaster.PLoS genetics · 2024Article
- Dose rate dependent reduction in chromatin accessibility at transcriptional start sites long time after exposure to gamma radiation.Epigenetics · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular DNA is constantly being damaged by numerous internal and external mutagenic factors. Probably the most severe type of insults DNA could suffer are the double-strand DNA breaks (DSBs). They sever both DNA strands and compromise genomic stability, causing deleterious chromosomal aberrations that are implicated in numerous maladies, including cancer. Not surprisingly, cells have evolved several DSB repair pathways encompassing hundreds of different DNA repair proteins to cope with this challenge. In eukaryotic cells, DSB repair is fulfilled in the immensely complex environment of the chromatin. The chromatin is not just a passive background that accommodates the multitude of DNA repair proteins, but it is a highly dynamic and active participant in the repair process. Chromatin alterations, such as changing patterns of histone modifications shaped by numerous histone-modifying enzymes and chromatin remodeling, are pivotal for proficient DSB repair. Dynamic chromatin changes ensure accessibility to the damaged region, recruit DNA repair proteins, and regulate their association and activity, contributing to DSB repair pathway choice and coordination. Given the paramount importance of DSB repair in tumorigenesis and cancer progression, DSB repair has turned into an attractive target for the development of novel anticancer therapies, some of which have already entered the clinic.
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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.