肠上皮化生在Barrett’s食管进展为食管腺癌中作用的研究进展  

Intestinal metaplasia in progression of Barrett’s esophagus to esophageal adenocarcinoma

作　　者：李海素 褚传莲[1] Hai-Su Li;Chuan-Lian Chu(Jinan Central Hospital,Jinan Key Translational Gastroenterology Laboratory,Jinan Digestive Diseases Clinical Research Center,Jinan 250013,Shandong Province,China)

机构地区：[1]济南市中心医院,济南市胃肠疾病转化重点实验室,济南市消化疾病临床研究中心,山东省济南市250013

出　　处：《世界华人消化杂志》2023年第2期41-47,共7页World Chinese Journal of Digestology

摘　　要：食管腺癌(esophageal adenocarcinoma,EAC)的发病率有逐年增加的趋势,EAC预后差,5年生存率不足20%.Barrett’s食管(barrett’sesophagus,BE)是目前唯一已知的EAC癌前病变,伴肠上皮化生(intestinal metaplasia,IM)的BE有更高的风险进展为EAC,探究IM的发生机制,寻找BE的针对性治疗靶点,成为预防肿瘤的重要措施.胆汁酸反流被认为是IM发生的重要因素,并促进BE向EAC进展,但胆汁反流诱导肠化、癌变的分子调节机制尚不清楚.本文就IM发生的环境、意义、细胞起源学说,胆汁反流的毒性作用以及IM向肿瘤进展的分子改变进行综述,旨在提高临床医师对BE中IM的认识,为早期干预BE和防治EAC提供证据.The incidence of esophageal adenocarcinoma(EAC)has been increasing year by year.The prognosis of EAC is poor,and the 5-year survival rate is less than 20%.Barrett’s esophagus(BE)is the only known precancerous lesion of EAC.BE with intestinal metaplasia(IM)has a higher risk of progressing to EAC.Exploring the mechanism of IM and finding targeted therapeutic targets for BE has become an important measure for tumor prevention.Bile acid reflux is considered an important factor in the occurrence of IM and promotes the progression of BE to EAC.However,the molecular regulatory mechanism of bile reflux induced IM and carcinogenesis remains unclear.This article reviews the environment,significance,and cell origin theory of IM,toxic effects of bile reflux,and molecular changes of IM progression to tumor,aiming to improve clinicians’understanding of IM in BE and provide evidence for early intervention of BE and prevention and treatment of EAC.

关 键 词：Barrett’s食管 肠上皮化生 胆汁酸 食管腺癌 表观遗传学 

分 类 号：R735.1[医药卫生—肿瘤]