Etiology and Pathophysiology of Barrett's Esophagus/Neoplasia.

IF 3.6 3区医学 Q2 GASTROENTEROLOGY & HEPATOLOGY

Digestion Pub Date : 2025-09-15 DOI:10.1159/000548413

Naoki Asano, Tomoyuki Koike, Masahiro Saito, Yutaka Hatayama, Yohei Ogata, Xiaoyi Jin, Takeshi Kanno, Waku Hatta, Kaname Uno, Akira Imatani, Atsushi Masamune

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引用次数: 0

Abstract

Background: Barrett's esophagus and its malignant progression to Barrett's adenocarcinoma are becoming increasingly prevalent worldwide, yet their underlying mechanisms remain incompletely understood.

Summary: The pathogenesis of Barrett's esophagus and Barrett's adenocarcinoma 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.

Key messages: The pathophysiological mechanisms underlying Barrett's esophagus and the development of Barrett's adenocarcinoma are still under active investigation. Understanding these mechanisms is essential for developing effective preventive and therapeutic strategies.

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Barrett食管/肿瘤的病因学和病理生理学。

Barrett食管及其恶性进展为Barrett腺癌在世界范围内越来越普遍，但其潜在机制仍不完全清楚。发病机制是多因素的，涉及环境、遗传和细胞因素。慢性酸和胆汁反流是公认的促进食管上皮细胞转化的因素。肥胖通过间接增加反流和直接通过促炎脂肪因子，进一步加剧了这种风险。最近的遗传学研究已经确定了几种遗传风险变异，p53的丧失被认为是恶性进展的关键事件。此外，Barrett食管的起源仍在研究中，可能的来源包括食管粘膜下腺细胞、贲门细胞和循环骨髓源细胞。了解这些机制对于制定有效的预防和治疗策略至关重要。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Digestion 医学-胃肠肝病学

CiteScore

7.90

自引率

0.00%

发文量

审稿时长

6-12 weeks

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.