Barretts's carcinogenesis.
Barret's esophagus
bile acid, gastroesophageal reflux, metaplasia
Journal
Pathology international
ISSN: 1440-1827
Titre abrégé: Pathol Int
Pays: Australia
ID NLM: 9431380
Informations de publication
Date de publication:
Jun 2019
Jun 2019
Historique:
received:
10
11
2018
accepted:
22
03
2019
pubmed:
11
7
2019
medline:
19
2
2020
entrez:
11
7
2019
Statut:
ppublish
Résumé
Barrett's esophagus is considered a precancerous lesion of esophageal adenocarcinoma (EAC). Long-segment Barrett's esophagus, which is generally associated with intestinal metaplasia, has a higher rate of carcinogenesis than short-segment Barrett's esophagus, which is mainly composed of cardiac-type mucosa. However, a large number of cases reportedly develop EAC from the cardiac-type mucosa which has the potential to involve intestinal phenotypes. There is no consensus regarding whether the definition of Barrett's epithelium should include intestinal metaplasia. Basic researches using rodent models have provided information regarding the origins of Barrett's epithelium. Nevertheless, it remains unclear whether differentiated gastric columnar epithelium or stratified esophageal squamous epithelium undergo transdifferentiation into the intestinal-type columnar epithelium, transcommittment into the columnar epithelium, or whether the other pathways exist. Reflux of duodenal fluid including bile acids into the stomach may occur when an individual lies down after eating, which could cause the digestive juices to collect in the fornix of the stomach. N-nitroso-bile acids are produced with nitrites that are secreted from the salivary glands, and bile acids can drive expression of pro-inflammatory cytokines via EGFR or the NF-κB pathway. These steps may contribute significantly to carcinogenesis.
Identifiants
pubmed: 31290583
doi: 10.1111/pin.12804
pmc: PMC6851828
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
319-330Informations de copyright
© 2019 The Authors. Pathology International published by the Japanese Society of Pathology and John Wiley & Sons Australia, Ltd.
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