ReviewDigestive diseases (Basel, Switzerland)
From Reflux Esophagitis to Esophageal Adenocarcinoma.
Review in Digestive diseases (Basel, Switzerland). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 79 citations in OpenAlex.
- A gene therapy approach to prevent dilated intercellular space, a hallmark of gastroesophageal reflux disease.Gene therapy · 2026Article
- Intrinsic mechanisms and microenvironmental cues fine-tune plasticity of esophageal progenitors.Nature communications · 2026Article
- VSIG10L is a major determinant of esophageal homeostasis and inherited predisposition to Barrett's esophagus.Nature communications · 2026Article
- Proteomic Profiling Informs Mechanisms of Esophageal Adenocarcinoma Inhibition by Cranberry Proanthocyanidins.Molecular nutrition & food research · 2025Article
- Integrated transcriptomic and metabolomic analyses reveal the mechanism by which quercetin inhibits reflux esophagitis in rats.PloS one · 2025Article
- Predicting the potential deterioration of Barrett's esophagus based on gut microbiota: a Mendelian randomization analysis.Mammalian genome : official journal of the International Mammalian Genome Society · 2024Article
- Gastro-Esophageal Junction Precancerosis: Histological Diagnostic Approach and Pathogenetic Insights.Cancers · 2023Review
- Article
- Signaling Pathways in the Pathogenesis of Barrett's Esophagus and Esophageal Adenocarcinoma.International journal of molecular sciences · 2023Review
- Role of Gastroesophageal Reflux Disease in Morbidity and Mortality for Patients Admitted With Pulmonary Hypertension.Cureus · 2023Article
- Columnar Metaplasia of the Esophagus Presenting as Iron Deficiency Anemia in Children with Neurologic Impairment or Congenital Esophageal Atresia.The American journal of case reports · 2022Review
- Bile reflux and hypopharyngeal cancer (Review).Oncology reports · 2021Review
- PDZK1 induces resistance to apoptosis in esophageal adenocarcinoma cells.Esophagus : official journal of the Japan Esophageal Society · 2021Article
- GATA4 blocks squamous epithelial cell gene expression in human esophageal squamous cells.Scientific reports · 2021Article
- Novel Ex Vivo Model to Examine the Mechanism and Relationship of Esophageal Microbiota and Disease.Biomedicines · 2021Article
- Bile Acids as a New Type of Steroid Hormones Regulating Nonspecific Energy Expenditure of the Body (Review).Sovremennye tekhnologii v meditsine · 2021Review
- Nanomedicine-based drug delivery towards tumor biological and immunological microenvironment.Acta pharmaceutica Sinica. B · 2020Review
- Article
- Scaphoid metastasis as the first sign of occult gastroesophageal junction cancer: A case report.World journal of clinical cases · 2020Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Reflux esophagitis causes Barrett's metaplasia, an abnormal esophageal mucosa predisposed to adenocarcinoma. Medical therapy for reflux esophagitis focuses on decreasing gastric acid production with proton pump inhibitors. We have reported that reflux esophagitis in a rat model develops from a cytokine-mediated inflammatory injury, not from a caustic chemical (acid) injury. In this model, refluxed acid and bile stimulate the release of inflammatory cytokines from esophageal squamous cells, recruiting lymphocytes first to the submucosa and later to the luminal surface. Emerging studies on acute reflux esophagitis in humans support this new concept, suggesting that reflux-induced cytokine release may be a future target for medical therapies. Sometimes, reflux esophagitis heals with Barrett's metaplasia, a process facilitated by reflux-related nitric oxide (NO) production and Sonic Hedgehog (Hh) secretion by squamous cells. We have shown that NO reduces expression of genes that promote a squamous cell phenotype, while Hh signaling induces genes that mediate the development of the columnar cell phenotypes of Barrett's metaplasia. Agents targeting esophageal NO production or Hh signaling conceivably could prevent the development of Barrett's esophagus. Persistent reflux promotes cancer in Barrett's metaplasia. We have reported that acid and bile salts induce DNA damage in Barrett's cells. Bile salts also cause NF-x03BA;B activation in Barrett's cells, enabling them to resist apoptosis in the setting of DNA damage and likely contributing to carcinogenesis. Oral treatment with ursodeoxycholic acid prevents the esophageal DNA damage and NF-x03BA;B activation induced by toxic bile acids. Altering bile acid composition might be another approach to cancer prevention.
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.