Barrett’s esophagus (BE) was initially defined in the 1950s as the visualization of gastric-like mucosa in the esophagus. Over time, the definition has evolved to include the identification of goblet cells, which confirm the presence of intestinal metaplasia within the esophagus. Chronic gastro-esophageal reflux disease (GERD) is a significant risk factor for adenocarcinoma of the esophagus, as intestinal metaplasia can develop due to GERD. The development of adenocarcinomas related to BE progresses in sequence from inflammation to metaplasia, dysplasia, and ultimately carcinoma. In the presence of GERD, the squamous epithelium changes to columnar epithelium, which initially lacks goblet cells, but later develops goblet cell metaplasia and eventually dysplasia. The accumulation of multiple genetic and epigenetic alterations leads to the development and progression of dysplasia. The diagnosis of BE requires the identification of intestinal metaplasia on histologic examination, which has thus become an essential tool both in the diagnosis and in the assessment of dysplasia’s presence and degree. The histologic diagnosis of BE dysplasia can be challenging due to sampling error, pathologists’ experience, interobserver variation, and difficulty in histologic interpretation: all these problems complicate patient management. The development and progression of Barrett’s esophagus (BE) depend on various molecular events that involve changes in cell-cycle regulatory genes, apoptosis, cell signaling, and adhesion pathways. In advanced stages, there are widespread genomic abnormalities with losses and gains in chromosome function, and DNA instability. This review aims to provide an updated and comprehensible diagnostic approach to BE based on the most recent guidelines available in the literature, and an overview of the pathogenetic and molecular mechanisms of its development.
巴雷特食管（BE）最初于20世纪50年代被定义为食管内出现胃型黏膜的可视化表现。随着时间推移，该定义已演变为包含杯状细胞的识别，这证实了食管内存在肠上皮化生。慢性胃食管反流病（GERD）是食管腺癌的重要危险因素，因为GERD可导致肠上皮化生的发生。与BE相关的腺癌发展按顺序从炎症进展为化生、异型增生，最终形成癌变。在GERD存在的情况下，鳞状上皮转变为柱状上皮，初期缺乏杯状细胞，随后发展为杯状细胞化生并最终形成异型增生。多种遗传和表观遗传改变的积累导致异型增生的发生与进展。BE的诊断需要通过组织学检查确认肠上皮化生的存在，这使得组织学检查成为诊断及评估异型增生存在与否及其程度的重要工具。由于取样误差、病理医师经验差异、观察者间变异以及组织学解读困难等因素，BE异型增生的组织学诊断具有挑战性：这些问题均使患者管理复杂化。巴雷特食管的发生与进展取决于多种分子事件，涉及细胞周期调控基因、细胞凋亡、细胞信号传导和黏附通路的变化。在晚期阶段，会出现广泛的基因组异常，包括染色体功能缺失与获得以及DNA不稳定性。本综述旨在基于文献中的最新指南，提供更新且易于理解的BE诊断方法，并概述其发病机制和分子生物学机制。
Gastro-Esophageal Junction Precancerosis: Histological Diagnostic Approach and Pathogenetic Insights
肿瘤(癌症)患者之家