Evidence map›Paper›PMID 32232911›Full record

ReviewCancer science2020

Relationship among DNA double-strand break (DSB), DSB repair, and transcription prevents genome instability and cancer.

Ayako Ui, Natsuko Chiba, Akira Yasui

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
5.9field-weighted citation impact, top 3% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

63 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
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  6. Airborne PMInternational journal of molecular sciences · 2025
    Article
  7. Histone Phosphorylation in DNA Damage Response.International journal of molecular sciences · 2025
    Review
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3 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Ayako UiGenome Regulation and Molecular Pharmacogenomics, School of Bioscience and Biotechnology, Tokyo University of Technology, Hachijoji, Japan.ORCID https://orcid.org/0000-0001-6698-7168
Natsuko ChibaDepartment of Cancer Biology, Institute of Development, Aging, and Cancer, Tohoku University, Sendai, Japan.
Akira YasuiDivision of Dynamic Proteome in Cancer and Aging, Institute of Development, Aging, and Cancer, Tohoku University, Sendai, Japan.
Tohoku University · JPTokyo University of Technology · JP

Funding

Japan Agency for Medical Research and Development 19cm0106605h0003Japan Society for the Promotion of Science 17K19615Naito FoundationPrincess Takamatsu Cancer Research FundTakeda Science Foundation
6 · The paper itself

Abstract

DNA double-strand break (DSB) is a serious type of DNA damage and is known to trigger multiple responses within cells. In these responses, novel relationships among DSB, DSB repair, and transcription machineries are created. First, transcription is repressed if DSB occurs near or at the transcription site, termed DSB-induced transcriptional repression, which contributes to DSB repair with the aid of DNA damage-signaling pathways, ATM- or DNA-PKcs-signaling pathways. DSB-induced transcriptional repression is also regulated by transcriptional factors TLP1, NELF, and ENL, as well as chromatin remodeling and organizing factors ZMYND8, CDYL1, PBAF, and cohesin. Second, transcription and RNA promote DSB repair for genome integrity. Transcription factors such as LEDGF, SETD2, and transcriptionally active histone modification, H3K36, facilitate homologous recombination to overcome DSB. At transcriptional active sites, DNA:RNA hybrids, termed R-loops, which are formed by DSB, are processed by RAD52 and XPG leading to an activation of the homologous recombination pathway. Even in a transcriptionally inactive non-genic sites, noncoding RNAs that are produced by RNA polymerase II, DICER, and DROSHA, help to recruit DSB repair proteins at the DSB sites. Third, transcriptional activation itself, however, can induce DSB. Transcriptional activation often generates specific DNA structures such as R-loops and topoisomerase-induced DSBs, which cause genotoxic stress and may lead to genome instability and consequently to cancer. Thus, transcription and DSB repair machineries interact and cooperate to prevent genome instability and cancer.

Indexed as

DNA Breaks, Double-StrandedDNA RepairTranscription, GeneticDNA DamageGenomic InstabilityHomologous RecombinationHumansNeoplasmsRNATranscriptional ActivationRNAcancerDSB repairgenome instabilityhomologous recombinationtranscription

Identifiers

PMID32232911
PMCPMC7226179
OpenAlexW3013766872

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.