ArticleNature communications2018
Mutation hotspots at CTCF binding sites coupled to chromosomal instability in gastrointestinal cancers.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 1 of them a synthesis that pooled 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.
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
99 citing papers in PubMed, 1 synthesis or guideline pooled it, 160 citations in OpenAlex.
- Global updates in the treatment of gastric cancer: a systematic review. Part 2: perioperative management, multimodal therapies, new technologies, standardization of the surgical treatment and educational aspects.Updates in surgery · 2020Pooled it
- CTCF-associated chromatin changes between HOXD1 and HOXD8 contribute to TNBC progression.Experimental & molecular medicine · 2026Article
- Novel MC1R variants cause red hair and lighter skin color.HGG advances · 2026Article
- Article
- Molecular characteristics and metastatic mechanism of patients diagnosed with Krukenberg tumor from gastric cancer.Journal of gastrointestinal oncology · 2026Article
- Therapy-associated mutagenesis at CTCF binding sites is shaped by chromatin context and DNA repair capacity.bioRxiv : the preprint server for biology · 2026Article
- Crosstalk BetweenCancers · 2026Review
- CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cells.iScience · 2026Article
- Identification of Novel Hub Genes and Potential Signaling Pathways with the Pathogenesis of Oral Cavity Squamous Cell Carcinoma Based on Bioinformatics Analysis.Cancer informatics · 2026Article
- Association of IL12RB2, RORC, and class II HLA polymorphisms with severe erythema multiforme of regorafenib in Japanese patients with colorectal cancer.Cancer chemotherapy and pharmacology · 2025Article
- Topoisomerase IIb binding delineates localized mutational processes and driver mutations in cancer genomes.Nature communications · 2025Article
- Non-coding RNAs-mediated regulation of the MAPK pathway in gastric cancer: translational perspectives.Discover oncology · 2025Review
- 3D Genome Constrains Breakpoints of Inversions That Can Act as Barriers to Gene Flow in the Stickleback.Molecular ecology · 2025Article
- Targeted inhibition of Ninjurin2 promotes chemosensitivity in chemoresistant gastric cancer by suppressing cancer-initiating cells.Biomarker research · 2025Article
- CTCF Point Mutation at R567 Disrupts Mouse Heart Development via 3D Genome Rearrangement and Transcription Dysregulation.Cell proliferation · 2025Article
- An overview of BAP1 biological functions and current therapeutics.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- Rethinking GWAS: how lessons from genetic screens and artificial intelligence could reveal biological mechanisms.Bioinformatics (Oxford, England) · 2025Article
- Big Data and Artificial Intelligence in Drug Discovery for Gastric Cancer: Current Applications and Future Perspectives.Current medicinal chemistry · 2025Review
- Somatic mosaicism in schizophrenia brains reveals prenatal mutational processes.Science (New York, N.Y.) · 2024Article
- ERCC2 mutations alter the genomic distribution pattern of somatic mutations and are independently prognostic in bladder cancer.Cell genomics · 2024Article
39 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
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tissue-specific driver mutations in non-coding genomic regions remain undefined for most cancer types. Here, we unbiasedly analyze 212 gastric cancer (GC) whole genomes to identify recurrently mutated non-coding regions in GC. Applying comprehensive statistical approaches to accurately model background mutational processes, we observe significant enrichment of non-coding indels (insertions/deletions) in three gastric lineage-specific genes. We further identify 34 mutation hotspots, of which 11 overlap CTCF binding sites (CBSs). These CBS hotspots remain significant even after controlling for a genome-wide elevated mutation rate at CBSs. In 3 out of 4 tested CBS hotspots, mutations are nominally associated with expression change of neighboring genes. CBS hotspot mutations are enriched in tumors showing chromosomal instability, co-occur with neighboring chromosomal aberrations, and are common in gastric (25%) and colorectal (19%) tumors but rare in other cancer types. Mutational disruption of specific CBSs may thus represent a tissue-specific mechanism of tumorigenesis conserved across gastrointestinal cancers.
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.