巴雷特食管的分子机制。
Molecular mechanisms of Barrett's esophagus.
机构信息
Cancer Research Program, Julius L. Chambers Biomedical Biotechnology Research Institute, North Carolina Central University, 700 George Street, Durham, NC 27707, USA.
出版信息
Dig Dis Sci. 2011 Dec;56(12):3405-20. doi: 10.1007/s10620-011-1885-6. Epub 2011 Oct 8.
Abstract
Barrett's esophagus (BE) is defined as the metaplastic conversion of esophageal squamous epithelium to intestinalized columnar epithelium. As a premalignant lesion of esophageal adenocarcinoma (EAC), BE develops as a result of chronic gastroesophageal reflux disease (GERD). Many studies have been conducted to understand the molecular mechanisms of this disease. This review summarizes recent results involving squamous and intestinal transcription factors, signaling pathways, stromal factors, microRNAs, and other factors in the development of BE. A conceptual framework is proposed to guide future studies. We expect elucidation of the molecular mechanisms of BE to help in the development of improved management of GERD, BE, and EAC.
摘要
巴雷特食管（BE）被定义为食管鳞状上皮向肠化生柱状上皮的化生。作为食管腺癌（EAC）的癌前病变，BE 是由于慢性胃食管反流病（GERD）发展而来。许多研究已经致力于理解这种疾病的分子机制。这篇综述总结了涉及鳞状和肠转录因子、信号通路、基质因子、microRNAs 以及 BE 发展过程中的其他因素的最新研究结果。提出了一个概念框架以指导未来的研究。我们期望阐明 BE 的分子机制有助于改善 GERD、BE 和 EAC 的管理。
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