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机构地区:[1]南京大学医学院临床学院(南京军区南京总医院)消化内科,南京医学硕士研究生210002
出 处:《医学研究生学报》2014年第3期307-312,共6页Journal of Medical Postgraduates
基 金:国家自然科学基金(81070289)
摘 要:食管腺癌(esophageal adenocarcinoma,EAC)的发病率在西方人群中显著增加,且其预后较差。其主要危险因素包括胃食管反流病(gastroesophageal reflux disease,GERD)和Barrett食管(Barrett esophagus,BE),两者均与食管鳞状上皮炎症密切相关。然而,促进EAC发展的细胞作用机制却知之甚少。BE中的慢性炎症建立了一个适于细胞DNA损伤和改变与细胞增殖和凋亡抑制相关的基因表达的微环境。炎症级联反应中的关键因素包括产生自由基,活化激酶通路和转录因子,生成细胞因子和炎性酶类。文中重点阐述反流诱导的炎症和EAC发生之间的联系。了解参与炎症相关的EAC发生的分子途径,可为EAC提供一个更好的靶向治疗方法。The incidence of esophageal adenocarcinoma is significantly increasing in Western populations, and patients with this cancer have a poor prognosis. The major risk factors are gastroesophageal reflux disease and Barrett's esophagus, both of which are associated with inflammation of the esophageal squamous epithelium. However, the cellular mechanisms contributing to cancer develop-ment in the esophagus are poorly understood. The chronic inflammation that is present in Barrett's esophagus creates a mieroenviron- ment suitable for DNA damage and altered expression of genes involved in cellular proliferation and inhibition of apoptosis. Key players in the inflammatory cascade include generation of free radicals, activation of kinases pathways and transcription factors, and production of cytokines and inflammatory enzymes. The current review highlights the link between reflux-induced inflammation and esophageal car-cinogenesis. Understanding the molecular pathways involved in inflammation-associated esophageal tumorigenesis could offer a better targeted therapeutic treatment in esophageal adenocarcinoma.
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