{"title":"Etiology and pathophysiology of Barrett's esophagus/neoplasia.","authors":"Naoki Asano, Tomoyuki Koike, Masahiro Saito, Yutaka Hatayama, Yohei Ogata, Xiaoyi Jin, Takeshi Kanno, Waku Hatta, Kaname Uno, Akira Imatani, Atsushi Masamune","doi":"10.1159/000548413","DOIUrl":null,"url":null,"abstract":"<p><p>Barrett's esophagus and its malignant progression to Barrett's adenocarcinoma are becoming increasingly prevalent worldwide, yet their underlying mechanisms remain incompletely understood. The pathogenesis is multifactorial, involving environmental, genetic, and cellular factors. Chronic acid and bile reflux are well-established contributors, promoting cellular transformation in the esophageal epithelium. Obesity further exacerbates this risk, both indirectly by increasing reflux and directly via proinflammatory adipokines. Recent genetic studies have identified several genetic risk variants, with loss of p53 recognized as critical event in malignant progression. Moreover, the origin of Barrett's esophagus remains under investigation, with proposed sources including cells of esophageal submucosal glands, cells of gastric cardia, and circulating bone marrow-derived cells. Understanding these mechanisms is essential for developing effective preventive and therapeutic strategies.</p>","PeriodicalId":11315,"journal":{"name":"Digestion","volume":" ","pages":"1-14"},"PeriodicalIF":3.6000,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Digestion","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1159/000548413","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Barrett's esophagus and its malignant progression to Barrett's adenocarcinoma are becoming increasingly prevalent worldwide, yet their underlying mechanisms remain incompletely understood. The pathogenesis is multifactorial, involving environmental, genetic, and cellular factors. Chronic acid and bile reflux are well-established contributors, promoting cellular transformation in the esophageal epithelium. Obesity further exacerbates this risk, both indirectly by increasing reflux and directly via proinflammatory adipokines. Recent genetic studies have identified several genetic risk variants, with loss of p53 recognized as critical event in malignant progression. Moreover, the origin of Barrett's esophagus remains under investigation, with proposed sources including cells of esophageal submucosal glands, cells of gastric cardia, and circulating bone marrow-derived cells. Understanding these mechanisms is essential for developing effective preventive and therapeutic strategies.
期刊介绍：
''Digestion'' concentrates on clinical research reports: in addition to editorials and reviews, the journal features sections on Stomach/Esophagus, Bowel, Neuro-Gastroenterology, Liver/Bile, Pancreas, Metabolism/Nutrition and Gastrointestinal Oncology. Papers cover physiology in humans, metabolic studies and clinical work on the etiology, diagnosis, and therapy of human diseases. It is thus especially cut out for gastroenterologists employed in hospitals and outpatient units. Moreover, the journal''s coverage of studies on the metabolism and effects of therapeutic drugs carries considerable value for clinicians and investigators beyond the immediate field of gastroenterology.
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