ArticleDigestive diseases and sciences2005
Expression of Cdx2 in early GRCL of Barrett's esophagus induced in rats by duodenal reflux.
Article in Digestive diseases and sciences, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- How to Define the Gastroesophageal Junction.Digestive endoscopy : official journal of the Japan Gastroenterological Endoscopy Society · 2026Review
- Article
- Bile Acid-Microbiome Interaction Promotes Gastric Carcinogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Essential roles of HDAC1 and 2 in lineage development and genome-wide DNA methylation during mouse preimplantation development.Epigenetics · 2020Article
- From genetics to signaling pathways: molecular pathogenesis of esophageal adenocarcinoma.Biochimica et biophysica acta. Reviews on cancer · 2019Review
- Roles of the hexosamine biosynthetic pathway and pentose phosphate pathway in bile acid-induced cancer development.Cancer science · 2019Article
- Host factors influence Barrett's carcinogenesis: findings from a mouse gastroduodenal reflux model.Esophagus : official journal of the Japan Esophageal Society · 2019Article
- Barretts's carcinogenesis.Pathology international · 2019Article
- Article
- Columnar Metaplasia in Three Types of Surgical Mouse Models of Esophageal Reflux.Cellular and molecular gastroenterology and hepatology · 2017Article
- Reflux esophagitis and its role in the pathogenesis of Barrett's metaplasia.Journal of gastroenterology · 2017Review
- Goblet Cell Ratio in Combination with Differentiation and Stem Cell Markers in Barrett Esophagus Allow Distinction of Patients with and without Esophageal Adenocarcinoma.Cancer prevention research (Philadelphia, Pa.) · 2017Article
- Article
- Barrett's Esophagus: A Comprehensive and Contemporary Review for Pathologists.The American journal of surgical pathology · 2016Review
- Esophageal Helicobacter pylori colonization aggravates esophageal injury caused by reflux.World journal of gastroenterology · 2014Article
- Relationships of CDXs and apical sodium-dependent bile acid transporter in Barrett's esophagus.World journal of gastroenterology · 2013Article
- [Barrett's esophagus: analyses from human and experimental animal studies].Der Pathologe · 2013Article
- Barrett esophagus: what a mouse model can teach us about human disease.Cell cycle (Georgetown, Tex.) · 2012Review
- Bile acid and inflammation activate gastric cardia stem cells in a mouse model of Barrett-like metaplasia.Cancer cell · 2012Article
- Barrett's esophagus and animal models.Annals of the New York Academy of Sciences · 2011Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The intestine-specific caudal-related homeobox transcription factor Cdx2 is widely accepted to play a key role in intestinal development and differentiation in mammals. We studied the role of Cdx2 in the development of Barrett's esophagus (BE). In previous studies, we have shown a sequence of morphological changes of squamous epithelium leading to BE, found a peculiar metaplastic change common to other parts of gut, and proposed the concept of a "gut regenerative cell lineage" (GRCL). The GRCL is characterized by pyloric-foveolar metaplasia with goblet cell metaplasia, which occurs in the regenerative process in response to chronic inflammation. BE very likely develops through the GRCL, and we studied the expression of Cdx2 in various lesions of rat esophageal mucosa induced by duodenal reflux, using reverse transciptase-polymerase chain reaction and immunohistochemistry against Cdx2. We found that Cdx2 was expressed not only in specialized columnar epithelium (SCE) of BE, but also in several pyloric gland and foveolar metaplastic cells which developed in the basal layer of the squamous epithelium at an earlier stage of SCE development. These findings indicate that Cdx2 plays a crucial role in directing intestinal-type differentiation of the GRCL.
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