ArticleNature genetics2019
Release of paused RNA polymerase II at specific loci favors DNA double-strand-break formation and promotes cancer translocations.
Article in Nature genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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
59 citing papers in PubMed, 110 citations in OpenAlex.
- Targeting CIC::DUX4 sarcoma with Minnelide in a dual recombinase-initiated genetically engineered mouse model.The Journal of clinical investigation · 2026Article
- Macrophages promote aberrant DNA repair in multiple myeloma via the CXCL5/8-CXCR2 axis.Haematologica · 2026Article
- Topoisomerase IIb binding delineates localized mutational processes and driver mutations in cancer genomes.Nature communications · 2025Article
- ChromInSight: Revealing DNA Double-Strand Breaks Through Chromatin Structural Insights With an Interpretable Graph Neural Network Framework.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Steroid-Modulated Transcription Synergistically Forms DNA Double-Strand Breaks With Topoisomerase II Inhibitor.Cancer science · 2025Article
- ANP32E drives vulnerability to ATR inhibitors by inducing R-loops-dependent transcription replication conflicts in triple negative breast cancer.Nature communications · 2025Article
- Identification of a novel TOP2B::AFF2 fusion gene in B-cell acute lymphoblastic leukemia.Scientific reports · 2025Article
- Methods and applications of genome-wide profiling of DNA damage and rare mutations.Nature reviews. Genetics · 2024Review
- CDK12-inactivation-induced MYC signaling causes dependency on the splicing kinase SRPK1.Molecular oncology · 2024Article
- The GC-content at the 5' ends of human protein-coding genes is undergoing mutational decay.Genome biology · 2024Article
- R-loop resolution by ARIP4 helicase promotes androgen-mediated transcription induction.Science advances · 2024Article
- Transcriptional pausing induced by ionizing radiation enables the acquisition of radioresistance in nasopharyngeal carcinoma.Journal of molecular cell biology · 2024Article
- DSB profiles in human spermatozoa highlight the role of TMEJ in the male germline.Frontiers in genetics · 2024Article
- To Break or Not to Break: The Role of TOP2B in Transcription.International journal of molecular sciences · 2023Review
- A graph neural network-based interpretable framework reveals a novel DNA fragility-associated chromatin structural unit.Genome biology · 2023Article
- DNA double-strand break end synapsis by DNA loop extrusion.Nature communications · 2023Article
- Article
- ATM suppresses c-Myc overexpression in the mammary epithelium in response to estrogen.Cell reports · 2023Article
- DNA replication initiation shapes the mutational landscape and expression of the human genome.Science advances · 2022Article
- Untangling the roles of TOP2A and TOP2B in transcription and cancer.Science advances · 2022Review
Corrections and comments
- Commented on by
Authors and funding
17 authors at 10 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is not clear how spontaneous DNA double-strand breaks (DSBs) form and are processed in normal cells, and whether they predispose to cancer-associated translocations. We show that DSBs in normal mammary cells form upon release of paused RNA polymerase II (Pol II) at promoters, 5' splice sites and active enhancers, and are processed by end-joining in the absence of a canonical DNA-damage response. Logistic and causal-association models showed that Pol II pausing at long genes is the main predictor and determinant of DSBs. Damaged introns with paused Pol II-pS5, TOP2B and XRCC4 are enriched in translocation breakpoints, and map at topologically associating domain boundary-flanking regions showing high interaction frequencies with distal loci. Thus, in unperturbed growth conditions, release of paused Pol II at specific loci and chromatin territories favors DSB formation, leading to chromosomal translocations.
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.