Signaling Pathways in the Pathogenesis of Barrett's Esophagus and Esophageal Adenocarcinoma

被引:9
作者
Maslenkina, Ksenia [1 ]
Mikhaleva, Liudmila [1 ]
Naumenko, Maxim [1 ]
Vandysheva, Rositsa [1 ]
Gushchin, Michail [1 ]
Atiakshin, Dmitri [2 ]
Buchwalow, Igor [2 ,3 ]
Tiemann, Markus [3 ]
机构
[1] Petrovsky Natl Res Ctr Surg, AP Avtsyn Res Inst Human Morphol, Moscow 119991, Russia
[2] Peoples Friendship Univ Russia, Res & Educ Resource Ctr Immunophenotyping, Digital Spatial Profiling & Ultrastruct Anal Innov, Moscow 117198, Russia
[3] Inst Hematopathol, Fangdieckstr 75a, D-22547 Hamburg, Germany
关键词
Barrett's esophagus; inflammatory signaling pathways; intestinal metaplasia; mutational load; p53; dysplasia; carcinogenesis; esophageal adenocarcinoma; OXIDATIVE DNA-DAMAGE; BILE-ACIDS; SQUAMOUS EPITHELIUM; REFLUX ESOPHAGITIS; NITRIC-OXIDE; CDX2; EXPRESSION; GENE-EXPRESSION; STEM-CELLS; RAT MODEL; METAPLASIA;
D O I
10.3390/ijms24119304
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Barrett's esophagus (BE) is a premalignant lesion that can develop into esophageal adenocarcinoma (EAC). The development of Barrett's esophagus is caused by biliary reflux, which causes extensive mutagenesis in the stem cells of the epithelium in the distal esophagus and gastro-esophageal junction. Other possible cellular origins of BE include the stem cells of the mucosal esophageal glands and their ducts, the stem cells of the stomach, residual embryonic cells and circulating bone marrow stem cells. The classical concept of healing a caustic lesion has been replaced by the concept of a cytokine storm, which forms an inflammatory microenvironment eliciting a phenotypic shift toward intestinal metaplasia of the distal esophagus. This review describes the roles of the NOTCH, hedgehog, NF-?B and IL6/STAT3 molecular pathways in the pathogenesis of BE and EAC.
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