ReviewCell2017
Endogenous DNA Damage as a Source of Genomic Instability in Cancer.
Review in Cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 875 papers, 1 of them a synthesis 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
875 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Broad repression of DNA repair genes in senescent cells identified by integration of transcriptomic data.Nucleic acids research · 2025Pooled it
- DNA Repair Mechanisms.Methods in molecular biology (Clifton, N.J.) · 2027Review
- Septins buffer actomyosin forces to protect the nucleus from genotoxic mechanical stress.The Journal of cell biology · 2026Article
- Alkylating Agent-Induced FANCL Impairment Damages Pulmonary Arterial, Venous, and Microvascular Endothelial Cells and Predisposes to PAH/PVOD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Genome stability disrupted by the circRBM39(4,5,6)-RPA2 axis represses breast tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- DNA end-resection is stimulated by an interaction between BRCA1 exon 11 and TOPBP1.EMBO reports · 2026Article
- Interplay Between Epigenetics and Reactive Oxygen Species in Tumor Radioresistance: Mechanisms and Therapeutic Strategies for Radiotherapy.Cancer medicine · 2026Review
- Persistent TOP1 cleavage complexes in drug-tolerant cells drive adaptive resistance to EGFR-targeted therapies in lung cancer.Science advances · 2026Article
- Single-cell mapping of chromosome breaks identifies multiple fragile site classes with distinct DNA replication timing landscapes.Nature communications · 2026Article
- PARylation at the Genome-Proteome Interface: Regulation of DNA Repair Protein Dynamics.International journal of molecular sciences · 2026Review
- Structural basis of PARP2 recognition of nucleosomal DNA breaks and inhibitor trapping.Nucleic acids research · 2026Article
- TALAVE in Breast Cancer:bioRxiv : the preprint server for biology · 2026Article
- Modulation of DNA Damage by Epstein-Barr Virus (EBV).Viruses · 2026Review
- Review
- Significance of p53-binding protein 1 as an in situ DNA damage marker for ulcerative colitis.Medical molecular morphology · 2026Article
- Loss of CYLD on Chromosome 16q Impairs Homologous Recombination and Genomic Stability Through TIRR Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Oligomeric State of Rad6-Rad18 and Its Interactions with Translesion Synthesis Proteins.Biomolecules · 2026Article
- Partitioning of parental histones between leading and lagging strands is modulated by DNA polymerase dosage.Nucleic acids research · 2026Article
- Oxidative stress triggers RNAPII arrest through PARylation and DNA damage.Nature communications · 2026Article
- G-quadruplex structures as regulators of cellular processes and drivers of genome instability in cancer.Critical reviews in biochemistry and molecular biology · 2026Review
815 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.
Funding
Abstract
Genome instability, defined as higher than normal rates of mutation, is a double-edged sword. As a source of genetic diversity and natural selection, mutations are beneficial for evolution. On the other hand, genomic instability can have catastrophic consequences for age-related diseases such as cancer. Mutations arise either from inactivation of DNA repair pathways or in a repair-competent background due to genotoxic stress from celluar processes such as transcription and replication that overwhelm high-fidelity DNA repair. Here, we review recent studies that shed light on endogenous sources of mutation and epigenomic features that promote genomic instability during cancer evolution.
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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.