Department of Gastroenterology, Royal Albert Edward Infirmary, Wigan Lane, Wigan, Greater Manchester WN12NN, United Kingdom.
World J Gastroenterol. 2011 Aug 28;17(32):3672-83. doi: 10.3748/wjg.v17.i32.3672.
Barrett's esophagus (BE) confers a significant increased risk for development of esophageal adenocarcinoma (EAC), with the pathogenesis appearing to progress through a "metaplasia-dysplasia-carcinoma" (MDC) sequence. Many of the genetic insults driving this MDC sequence have recently been characterized, providing targets for candidate biomarkers with potential clinical utility to stratify risk in individual patients. Many clinical risk factors have been investigated, and associations with a variety of genetic, specific gastrointestinal and other modifiable factors have been proposed in the literature. This review summarizes the current understanding of the mechanisms involved in neoplastic progression of BE to EAC and critically appraises the relative roles and contributions of these putative risk factors from the published evidence currently available.
巴雷特食管(BE)显著增加了食管腺癌(EAC)的发病风险,其发病机制似乎是通过“化生-异型增生-癌”(MDC)序列进行的。最近已经对许多推动 MDC 序列的遗传损伤进行了描述,为候选生物标志物提供了目标,这些标志物具有潜在的临床应用价值,可以对个体患者的风险进行分层。已经研究了许多临床危险因素,并且在文献中提出了与多种遗传、特定胃肠道和其他可改变因素的关联。这篇综述总结了目前对 BE 向 EAC 肿瘤进展所涉及的机制的理解,并根据目前可用的已发表证据,批判性地评估了这些假定危险因素的相对作用和贡献。