Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Signaling Pathways in Pathogenesis of Barrett’s Esophagus and Esophageal Adenocarcinoma

Version 1 : Received: 25 April 2023 / Approved: 26 April 2023 / Online: 26 April 2023 (15:01:48 CEST)

A peer-reviewed article of this Preprint also exists.

Maslenkina, K.; Mikhaleva, L.; Naumenko, M.; Vandysheva, R.; Gushchin, M.; Atiakshin, D.; Buchwalow, I.; Tiemann, M. Signaling Pathways in the Pathogenesis of Barrett’s Esophagus and Esophageal Adenocarcinoma. Int. J. Mol. Sci. 2023, 24, 9304. Maslenkina, K.; Mikhaleva, L.; Naumenko, M.; Vandysheva, R.; Gushchin, M.; Atiakshin, D.; Buchwalow, I.; Tiemann, M. Signaling Pathways in the Pathogenesis of Barrett’s Esophagus and Esophageal Adenocarcinoma. Int. J. Mol. Sci. 2023, 24, 9304.

Abstract

Barrett’s esophagus (BE) is a premalignant lesion for esophageal adenocarcinoma (EAC). Development of Barrett’s esophagus is caused by biliary reflux that provokes intensive mutagenesis in stem cells of epithelium in distal esophagus and gastro-esophageal junction. Other possible cell origins of Barrett’s esophagus include stem cells of mucosal esophageal glands and their ducts, of stomach, residual embryonic cells and circulating bone marrow stem cells. Classic conception of healing of caustic lesion was replaced by idea of cytokine storm that forms inflammatory microenvironment for phenotypic shift toward intestinal metaplasia of distal esophagus. The review summarizes contemporary concepts of BE and EAC pathogenesis.

Keywords

Barrett’s esophagus; inflammatory signaling pathways; intestinal metaplasia; mutational load; p53; dysplasia; carcinogenesis; esophageal adenocarcinoma

Subject

Public Health and Healthcare, Public Health and Health Services

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