摘要
食管腺癌是一种高度恶性肿瘤,尽管在诊断和治疗方面取得了进步,但食管腺癌的治疗效果仍然较差,预后不佳。因此有必要探讨这种疾病发生发展的分子机制。食管黏膜上皮在反流内容物胃酸和胆汁的刺激下释放细胞因子,诱导炎症细胞迁移,迁移的炎症细胞进一步释放炎症细胞因子,损害食管黏膜,导致食管炎症,若是刺激因素长期存在导致炎症迁延不愈,就会形成慢性炎症。慢性炎症中伴随炎症细胞、细胞因子的转变,激活炎症通路,形成适合肿瘤发生、增殖、侵袭、转移的肿瘤微环境,在食管的炎症-化生-腺癌的转变中发挥重要作用,所以弄清炎症与食管腺癌发生发展的关系,可为食管腺癌的防治提供新思路。
Esophageal adenocarcinoma is a highly malignant tumor.Although it has made progress in the diagnosis and treatment,esophageal adenocarcinoma has poor therapeutic effect and poor prognosis.Therefore,it is necessary to explore the molecular mechanism of the disease development.The esophageal mucosa epithelium releases inflammatory cytokines under the stimulation of gastric acid and bile in the reflux content,and induces inflammatory cell migration.The migrated inflammatory cells further release inflammatory cytokines,damage the esophageal mucosa,and produce esophageal inflammation.If the stimulating factors persist for a long time,it may cause the inflammation to prolong and form chronic inflammation.Chronic inflammation is accompanied by activation and migration of inflammatory cells,releasing a variety of cytokines,activating inflammatory pathways,forming the tumor microenvironment suitable for tumorigenesis,proliferation,invasion,and metastasis,which play an important role in the transformation of the esophagus inflammation-metaplastic-adenocarcinoma.Therefore,understanding the relationship between inflammation and the development of esophageal adenocarcinoma,can provide newideas for the prevention and treatment of esophageal adenocarcinoma.
作者
胡有珍
潘玉琼
王瑞华
HU Youzhen;POON Karen;WANG Ruihua(Department of Gastroenterology,Shenzhen Hospital of Southern Medical University,Shenzhen 518100,China;Program of Food Science and Technology,Division of Science and Technology,BNU-HKBU United International College,Zhuhai 519085,China)
出处
《医学综述》
2019年第22期4449-4453,4458,共6页
Medical Recapitulate
关键词
慢性炎症
食管腺癌
BARRETT食管
炎症细胞
细胞因子
信号转导及转录激活因子3
核因子ΚB
抗炎治疗
Chronic inflammation
Esophageal adenocarcinoma
Barrett′s esophagus
Inflammatory cells
Cytokines
Signal transduction and transcription activator 3
Nuclear factor-κB
Anti-inflammatory therapy