ArticleOncogene2014
Next-generation sequencing of endoscopic biopsies identifies ARID1A as a tumor-suppressor gene in Barrett's esophagus.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 3 of them syntheses that pooled it.
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Who cites it
57 citing papers in PubMed, 3 syntheses or guidelines pooled it, 99 citations in OpenAlex.
- Genetic Biomarkers of Barrett's Esophagus Susceptibility and Progression to Dysplasia and Cancer: A Systematic Review and Meta-Analysis.Digestive diseases and sciences · 2016Pooled it
- Prognostic role and implications of mutation status of tumor suppressor gene ARID1A in cancer: a systematic review and meta-analysis.Oncotarget · 2015Pooled it
- A systematic review and meta-analysis of somatic and germline DNA sequence biomarkers of esophageal cancer survival, therapy response and stage.Annals of oncology : official journal of the European Society for Medical Oncology · 2015Pooled it
- MicroRNA-663a upregulation upon ARID1A depletion promotes the growth and migration of esophageal cancer cells by targeting FKBP8.Translational cancer research · 2026Article
- Current Concepts for Diagnosing Non-Dysplastic and Dysplastic Barrett's Esophagus.Gastrointestinal endoscopy clinics of North America · 2026Review
- The Interplay Between Esophageal Adenocarcinoma and Its Tumor Microenvironment: Toward Innovative Therapies.Cells · 2025Review
- Molecular interplay of ARID1A in gastrointestinal cancers.Medical oncology (Northwood, London, England) · 2025Review
- Article
- ISG15/GRAIL1/CD3 axis influences survival of patients with esophageal adenocarcinoma.JCI insight · 2024Article
- Article
- Epigenetics as a mediator of plasticity in cancer.Science (New York, N.Y.) · 2023Review
- Latest advances in the study of non-coding RNA-mediated circadian rhythm disorders causing endometrial cancer.Frontiers in oncology · 2023Review
- A nomogram and risk classification model predicts prognosis in Chinese esophageal squamous cell carcinoma patients.Translational cancer research · 2022Article
- Comparative genomic analysis of esophageal squamous cell carcinoma and adenocarcinoma: New opportunities towards molecularly targeted therapy.Acta pharmaceutica Sinica. B · 2022Review
- Co-existing TP53 and ARID1A mutations promote aggressive endometrial tumorigenesis.PLoS genetics · 2021Article
- Genetic profiles of Barrett's esophagus and esophageal adenocarcinoma in Japanese patients.Scientific reports · 2021Article
- Comprehensive Analysis of Barrett's Esophagus: Focused on Carcinogenic Potential for Barrett's Cancer in Japanese Patients.Digestive diseases and sciences · 2021Article
- The Role ofFrontiers in oncology · 2021Review
- Barrett's Esophagus and Esophageal Adenocarcinoma Biomarkers.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2020Article
- Identification of critical radioresistance genes in esophageal squamous cell carcinoma by whole-exome sequencing.Annals of translational medicine · 2020Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
The incidence of Barrett's esophagus (BE)-associated esophageal adenocarcinoma (EAC) is increasing. Next-generation sequencing (NGS) provides an unprecedented opportunity to uncover genomic alterations during BE pathogenesis and progression to EAC, but treatment-naive surgical specimens are scarce. The objective of this study was to establish the feasibility of using widely available endoscopic mucosal biopsies for successful NGS, using samples obtained from a BE 'progressor'. Paired-end whole-genome NGS was performed on the Illumina platform using libraries generated from mucosal biopsies of normal squamous epithelium (NSE), BE and EAC obtained from a patient who progressed to adenocarcinoma during endoscopic surveillance. Selective validation studies, including Sanger sequencing, immunohistochemistry and functional assays, were performed to confirm the NGS findings. NGS identified somatic nonsense mutations of AT-rich interactive domain 1A (SWI like) (ARID1A) and PPIE and an additional 37 missense mutations in BE and/or EAC, which were confirmed by Sanger sequencing. ARID1A mutations were detected in 15% (3/20) high-grade dysplasia (HGD)/EAC patients. Immunohistochemistry performed on an independent archival cohort demonstrated ARID1A protein loss in 0% (0/76), 4.9% (2/40), 14.3% (4/28), 16.0% (8/50) and 12.2% (12/98) of NSE, BE, low-grade dysplasia, HGD and EAC tissues, respectively, and was inversely associated with nuclear p53 accumulation (P=0.028). Enhanced cell growth, proliferation and invasion were observed on ARID1A knockdown in EAC cells. In addition, genes downstream of ARID1A that potentially contribute to the ARID1A knockdown phenotype were identified. Our studies establish the feasibility of using mucosal biopsies for NGS, which should enable the comparative analysis of larger 'progressor' versus 'non-progressor' cohorts. Further, we identify ARID1A as a novel tumor-suppressor gene in BE pathogenesis, reiterating the importance of aberrant chromatin in the metaplasia-dysplasia sequence.
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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.