ReviewNucleus (Austin, Tex.)2017
A meeting at risk: Unrepaired DSBs go for broke.
Review in Nucleus (Austin, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 10 citations in OpenAlex.
- Update on R-loops in genomic integrity: Formation, functions, and implications for human diseases.Genes & diseases · 2025Review
- Sites of chromosomal instability in the context of nuclear architecture and function.Cellular and molecular life sciences : CMLS · 2021Review
- Tracking telomere fusions through crisis reveals conflict between DNA transcription and the DNA damage response.NAR cancer · 2021Article
- The Secret Life of Chromosome Loops upon DNA Double-Strand Break.Journal of molecular biology · 2020Review
- Complex Chromatin Motions for DNA Repair.Frontiers in genetics · 2020Review
- A cohesin/HUSH- and LINC-dependent pathway controls ribosomal DNA double-strand break repair.Genes & development · 2019Article
- Review
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
Translocations are dramatic genomic rearrangements due to aberrant rejoining of distant DNA ends that can trigger cancer onset and progression. Translocations frequently occur in genes, yet the mechanisms underlying their formation remain poorly understood. One potential mechanism involves DNA Double Strand Break mobility and juxtaposition (i.e. clustering), an event that has been intensively debated over the past decade. Using Capture Hi-C, we recently found that DSBs do in fact cluster in human nuclei but only when induced in transcriptionally active genes. Notably, we found that clustering of damaged genes is regulated by cell cycle progression and coincides with damage persistency. Here, we discuss the mechanisms that could sustain clustering and speculate on the functional consequences of this seemingly double edge sword mechanism that may well stand at the heart of translocation biogenesis.
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.