ReviewNature reviews. Cancer2013
End-joining, translocations and cancer.
Review in Nature reviews. Cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 218 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
218 citing papers in PubMed, 352 citations in OpenAlex.
- DDX3X regulates DNA repair pathway choice at double-strand breaks via RNA-DNA hybrid formation.Cell death and differentiation · 2026Article
- Sam68 stimulates polymerase theta-mediated end-joining by suppressing poison exon inclusion in Polq mRNA.Nucleic acids research · 2026Article
- ACSF2 Functions as a regulatory switch for PARP inhibitor sensitivity in platinum-sensitive and homologous recombination-proficient high-grade serous ovarian cancer.Cancer cell international · 2026Article
- ESR1 fusion proteins in breast cancer: distinguishing oncogenic drivers from passenger events.Oncogene · 2026Review
- Novel AAV843 Vector-Mediated Gene Replacement Therapy Rescues Primary Hyperoxaluria Type I in Mice.Cells · 2026Article
- [Mefloquine HCl promotes DNA repair and alleviates radiation-induced lung epithelial cell injury].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- ERCC6L2 ensures repair fidelity for staggered-end DNA double-strand breaks.Nature communications · 2026Article
- Next Generation DNA Damage Response Inhibitors: Harnessing Nanocarriers and Tumor Microenvironment for Precision Cancer Therapy.Oncology research · 2026Review
- Review
- A nucleoskeleton network preserves genomic integrity by promoting NHEJ and restraining chromosome translocations.Nucleic acids research · 2025Article
- CRISPR/Cas9 generated DSB clusters mimic complex lesions induced by high-LET radiation and shift repair from c-NHEJ to mutagenic repair pathways.Scientific reports · 2025Article
- Crystal structure of the folded domains of Xrs2 from Saccharomyces cerevisiae.Acta crystallographica. Section F, Structural biology communications · 2025Article
- Genome rearrangements induced by the stimulation of end-joining of DNA double strand breaks through multiple phosphorylation of MRE11 by the kinase PKB/AKT1.Nucleic acids research · 2025Article
- Formation of multiple G-quadruplexes contributes toward BCR fragility associated with chronic myelogenous leukemia.Nucleic acids research · 2025Article
- Single-molecule techniques in studying the molecular mechanisms of DNA synapsis in non-homologous end-joining repair.Biophysics reports · 2025Article
- The Spiral Model of Evolution: Stable Life Forms of Organisms and Unstable Life Forms of Cancers.International journal of molecular sciences · 2024Review
- 53BP1 loss elicits cGAS-STING-dependent antitumor immunity in ovarian and pancreatic cancer.Nature communications · 2024Article
- High-complexity of DNA double-strand breaks is key for alternative end-joining choice.Communications biology · 2024Article
- Microhomology-mediated repair machinery and its relationship with HPV-mediated oncogenesis.Journal of medical virology · 2024Review
- Somatic structural variation signatures in pediatric brain tumors.Cell reports · 2023Article
158 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 at 2 institutions in 1 country.
Funding
Abstract
Fusion genes that are caused by chromosome translocations have been recognized for several decades as drivers of deregulated cell growth in certain types of cancer. In recent years, oncogenic fusion genes have been found in many haematological and solid tumours, demonstrating that translocations are a common cause of malignancy. Sequencing approaches have now confirmed that numerous, non-clonal translocations are a typical feature of cancer cells. These chromosome rearrangements are often highly complex and contain DNA sequence from multiple genomic sites. The factors and pathways that promote translocations are becoming clearer, with non-homologous end-joining implicated as a key source of genomic rearrangements.
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.