ReviewTrends in cell biology2016
Repair Pathway Choices and Consequences at the Double-Strand Break.
Review in Trends in cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 939 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.
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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.
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Who cites it
939 citing papers in PubMed.
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- Precision gene editing in infant neuroblastoma: a review of nanoparticle: enabled CRISPR/Cas9 therapies.Molecular biology reports · 2026Review
- CRISPR/Cas9-based nanodelivery systems for precision gene editing in neuroinflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- The ribonuclease ZC3H12A stabilizes BRCA1 mRNA in DNA damage response.Redox biology · 2026Article
- Interfering with DNA repair pathways to enhance CRISPR-Cas9-mediated homology-directed repair in a chelicerate genetic model.iScience · 2026Article
- Transgenerational chromosome repair in the asexual bdelloid rotiferScience advances · 2026Article
- GSK3β and Plk1 sequentially phosphorylate ATP-citrate lyase to promote homologous recombination.Science advances · 2026Article
- The DNA damage response and cancer immunotherapy.Nature reviews. Cancer · 2026Review
- Nucleases and Their Inhibitors: Exploring Biological Roles, Industrial Applications, and Challenges in Heterologous Expression.Biotechnology journal · 2026Review
- Tracking-seq: a universal off-target detection approach for CRISPR-Cas genome editing.Nature protocols · 2026Review
- Repair of DNA double-strand breaks after low radiation doses in childhood cancer survivors and matched cancer-free individuals.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Loss of CYLD on Chromosome 16q Impairs Homologous Recombination and Genomic Stability Through TIRR Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Genomic landscape of ERCC alterations in breast and gynecological cancers: implications for targeted therapy and VUS reclassification.Molecular biology reports · 2026Article
- Antibiotic-Induced Genotoxicity: Molecular Mechanisms, Cytogenetic Damage, and Implications for Human Health.International journal of molecular sciences · 2026Review
- Defective microhomology-mediated end joining inScience advances · 2026Article
- SPOP-mediated nuclear ubiquitination degradation of p62/SQSTM1 contributes to HR repair.Oncogene · 2026Article
- Article
- RAD51 in Breast Cancer: From Vulnerability to Resistance.World journal of oncology · 2026Review
- HAMNO and CGK733 as BRCAness-driven candidates exhibit synthetic lethality with olaparib in BRCA-proficient ovarian cancer.NPJ precision oncology · 2026Article
- CDW19S coordinates phasic end processing via distinct enzymatic activities.Nucleic acids research · 2026Article
879 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
3 authors.
Funding
Abstract
DNA double-strand breaks (DSBs) are cytotoxic lesions that threaten genomic integrity. Failure to repair a DSB has deleterious consequences, including genomic instability and cell death. Indeed, misrepair of DSBs can lead to inappropriate end-joining events, which commonly underlie oncogenic transformation due to chromosomal translocations. Typically, cells employ two main mechanisms to repair DSBs: homologous recombination (HR) and classical nonhomologous end joining (C-NHEJ). In addition, alternative error-prone DSB repair pathways, namely alternative end joining (alt-EJ) and single-strand annealing (SSA), have been recently shown to operate in many different conditions and to contribute to genome rearrangements and oncogenic transformation. Here, we review the mechanisms regulating DSB repair pathway choice, together with the potential interconnections between HR and the annealing-dependent error-prone DSB repair pathways.
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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.