ArticleGastroenterology2018
Detection of Mutations in Barrett's Esophagus Before Progression to High-Grade Dysplasia or Adenocarcinoma.
Article in Gastroenterology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.
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Who cites it
90 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Aberrant p53 Immunostaining in Barrett's Esophagus Predicts Neoplastic Progression: Systematic Review and Meta-Analyses.Digestive diseases and sciences · 2019Pooled it
- A machine-learning informed circulating microbial DNA signature for early diagnosis of esophageal adenocarcinoma.Gut microbes · 2026Article
- Article
- Biomarker Use in Barrett's Esophagus Surveillance.The American journal of gastroenterology · 2026Review
- Spatially resolved transcriptomic and proteomic profiling reveals cell interaction programs that predict Barrett's esophagus progression.bioRxiv : the preprint server for biology · 2026Article
- Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026Review
- Early Cancer Detection: What's Going on and What's Next.MedComm · 2026Review
- Molecular stratification of esophageal adenocarcinoma: implications for prognosis and treatment strategy.Oncogene · 2026Review
- Ultra-deep duplex sequencing reveals unique features of somatic evolution in the normal tissues of a family with Li-Fraumeni syndrome.bioRxiv : the preprint server for biology · 2026Article
- Emerging Biomarkers for Managing Barrett's Esophagus.Gastrointestinal endoscopy clinics of North America · 2026Review
- Current Concepts for Diagnosing Non-Dysplastic and Dysplastic Barrett's Esophagus.Gastrointestinal endoscopy clinics of North America · 2026Review
- Gastric (Foveolar)-Type Dysplasia in Barrett's Esophagus: A Clinical, Molecular, and Long-Term Outcome Study.The American journal of gastroenterology · 2025Article
- HPV status shapes T-cell immunoprofiles in oesophageal adenocarcinoma: high regulatory T cell infiltration predicts poor prognosis.Journal of translational medicine · 2025Article
- Concerted changes in Epithelium and Stroma: a multi-scale, multi-omics analysis of progression from Barrett's Esophagus to adenocarcinoma.Developmental cell · 2025Article
- Review
- Article
- Context-dependent effects of CDKN2A and other 9p21 gene losses during the evolution of esophageal cancer.Nature cancer · 2025Article
- Targeting Esophageal Cancer: Promising Drugs for the Clinical Landscape and Key Knowledge Gaps.Drug design, development and therapy · 2025Review
- Origins of cancer: ain't it just mature cells misbehaving?The EMBO journal · 2024Review
- The Aberrant Expression of Biomarkers and Risk Prediction for Neoplastic Changes in Barrett's Esophagus-Dysplasia.Cancers · 2024Article
30 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
BACKGROUND &
aimsBarrett's esophagus (BE) is the greatest risk factor for esophageal adenocarcinoma (EAC), but only a small proportion of patients with BE develop cancer. Biomarkers might be able to identify patients at highest risk of progression. We investigated genomic differences in surveillance biopsies collected from patients whose BE subsequently progressed compared to patients whose disease did not progress.
methodsWe performed a retrospective case-control study of 24 patients with BE that progressed to high-grade dysplasia (HGD, n = 14) or EAC (n = 10). The control group (n = 73, called non-progressors) comprised patients with BE and at least 5 years of total endoscopic biopsy surveillance without progression to HGD or EAC. From each patient, we selected a single tissue sample obtained more than 1 year before progression (cases) or more than 2 years before the end of follow-up (controls). Pathogenic mutations, gene copy numbers, and ploidy were compared between samples from progressors and non-progressors.
resultsTP53 mutations were detected in 46% of samples from progressors and 5% of non-progressors. In this case-control sample set, TP53 mutations in BE tissues increased the adjusted risk of progression 13.8-fold (95% confidence interval, 3.2-61.0) (P < .001). We did not observe significant differences in ploidy or copy-number profile between groups. We identified 147 pathogenic mutations in 57 distinct genes-the average number of pathogenic mutations was higher in samples from progressors (n = 2.5) than non-progressors (n = 1.2) (P < .001). TP53 and other somatic mutations were recurrently detected in samples with limited copy-number changes (aneuploidy).
conclusionsIn genomic analyses of BE tissues from patients with or without later progression to HGD or EAC, we found significantly higher numbers of TP53 mutations in BE from patients with subsequent progression. These mutations were frequently detected before the onset of dysplasia or substantial changes in copy number.
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