ArticleGut2017
Germline variation in inflammation-related pathways and risk of Barrett's oesophagus and oesophageal adenocarcinoma.
Article in Gut, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Sex-Specific Genetic Associations for Barrett's Esophagus and Esophageal Adenocarcinoma.Gastroenterology · 2020Pooled it
- Pathogenesis of Barrett's Esophagus: Evolving and Emerging Mechanisms.Gastrointestinal endoscopy clinics of North America · 2026Review
- Regulatory mechanisms of m6A RNA methylation in esophageal cancer: a comprehensive review.Frontiers in genetics · 2025Review
- Unraveling the pathogenesis of Barrett's esophagus and esophageal adenocarcinoma: the "omics" era.Frontiers in oncology · 2024Review
- Review
- Association or causation: still more questions than answers in early-onset gastrointestinal cancers.ESMO gastrointestinal oncology · 2023Article
- Article
- Refined expression quantitative trait locus analysis on adenocarcinoma at the gastroesophageal junction reveals susceptibility and prognostic markers.Frontiers in genetics · 2023Article
- High expression of cuproptosis-related gene FDX1 in relation to good prognosis and immune cells infiltration in colon adenocarcinoma (COAD).Journal of cancer research and clinical oncology · 2023Article
- A risk variant for Barrett's esophagus and esophageal adenocarcinoma at chr8p23.1 affects enhancer activity and implicates multiple gene targets.Human molecular genetics · 2022Article
- The roles of RNA NHeliyon · 2022Review
- eQTL Set-Based Association Analysis Identifies Novel Susceptibility Loci for Barrett Esophagus and Esophageal Adenocarcinoma.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2022Article
- Mechanisms and pathophysiology of Barrett oesophagus.Nature reviews. Gastroenterology & hepatology · 2022Review
- Today's Mistakes and Tomorrow's Wisdom in Development and Use of Biomarkers for Barrett's Esophagus.Visceral medicine · 2022Review
- Prioritization and functional analysis of GWAS risk loci for Barrett's esophagus and esophageal adenocarcinoma.Human molecular genetics · 2022Article
- Intrinsic Cellular Susceptibility to Barrett's Esophagus in Adults Born with Esophageal Atresia.Cancers · 2022Article
- Article
- Germline variation in the insulin-like growth factor pathway and risk of Barrett's esophagus and esophageal adenocarcinoma.Carcinogenesis · 2021Observational
- Association of Inflammation-Related Gene Polymorphisms With Susceptibility and Radiotherapy Sensitivity in Head and Neck Squamous Cell Carcinoma Patients in Northeast China.Frontiers in oncology · 2021Article
- Epidemiology of esophageal cancer: update in global trends, etiology and risk factors.Clinical journal of gastroenterology · 2020Review
Corrections and comments
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Authors and funding
40 authors.
Funding
Abstract
objectiveOesophageal adenocarcinoma (OA) incidence has risen sharply in Western countries over recent decades. Local and systemic inflammation is considered an important contributor to OA pathogenesis. Established risk factors for OA and its precursor, Barrett's oesophagus (BE), include symptomatic reflux, obesity and smoking. The role of inherited genetic susceptibility remains an area of active investigation. Here, we explore whether germline variation related to inflammatory processes influences susceptibility to BE/OA.
designWe used data from a genomewide association study of 2515 OA cases, 3295 BE cases and 3207 controls. Our analysis included 7863 single-nucleotide polymorphisms (SNPs) in 449 genes assigned to five pathways: cyclooxygenase (COX), cytokine signalling, oxidative stress, human leucocyte antigen and nuclear factor-κB. A principal components-based analytic framework was employed to evaluate pathway-level and gene-level associations with disease risk.
resultsWe identified a significant signal for the COX pathway in relation to BE risk (p=0.0059, false discovery rate q=0.03), and in gene-level analyses found an association with microsomal glutathione-S-transferase 1 (
conclusionsThis study provides the most comprehensive evaluation of inflammation-related germline variation in relation to risk of BE/OA and suggests that variants in
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