ArticleSurgery2009
Pathogenesis of Barrett's esophagus: bile acids inhibit the Notch signaling pathway with induction of CDX2 gene expression in human esophageal cells.
Article in Surgery, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Cell culture models for studying the development of Barrett's esophagus: a systematic review.Cellular oncology (Dordrecht, Netherlands) · 2012Pooled it
- Transcriptomic Profiling of Laser Capture Microdissected FFPE Esophageal Tissues Identifies Candidate Genes and Pathways Associated with Esophageal Adenocarcinoma.International journal of molecular sciences · 2026Article
- Captivating Synergistic, Dose-Dependent Anticancer Effects of Tumor-Regulation Modulators Chloroquine and Ivermectin Completely Abolished by an Opposing Modulator, Deoxycholic Acid, in Hamster Fibrosarcoma: In Vivo, In Vitro, and Literature Review.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Targeting notch signaling pathway in esophageal cancer: from molecular insights to therapies.Oncology reviews · 2026Review
- Development of a novel oncolytic adenovirus controlled by CDX2 promoter for esophageal adenocarcinoma therapy.Journal of gastroenterology · 2024Article
- Gut Microbiota, Human Blood Metabolites, and Esophageal Cancer: A Mendelian Randomization Study.Genes · 2024Article
- Signaling Pathways in the Pathogenesis of Barrett's Esophagus and Esophageal Adenocarcinoma.International journal of molecular sciences · 2023Review
- The role of bile acid in intestinal metaplasia.Frontiers in physiology · 2023Review
- The role of bile acids in carcinogenesis.Cellular and molecular life sciences : CMLS · 2022Review
- NOTCH and Esophageal Squamous Cell Carcinoma.Advances in experimental medicine and biology · 2021Review
- Notch Signaling Pathway Is Inhibited in the Development of Barrett's Esophagus: An In Vivo and In Vitro Study.Canadian journal of gastroenterology & hepatology · 2018Article
- Longitudinal study of esophageal mucosal damage after esophagectomy and gastric interposition: relationship between reflux-related mucosal injury and Notch signaling.Journal of thoracic disease · 2017Article
- Bile salt receptor TGR5 is highly expressed in esophageal adenocarcinoma and precancerous lesions with significantly worse overall survival and gender differences.Clinical and experimental gastroenterology · 2017Article
- Deoxycholic acid (DCA) confers an intestinal phenotype on esophageal squamous epithelium via induction of the stemness-associated reprogramming factors OCT4 and SOX2.Cell cycle (Georgetown, Tex.) · 2016Article
- Bile acids induce Delta-like 1 expression via Cdx2-dependent pathway in the development of Barrett's esophagus.Laboratory investigation; a journal of technical methods and pathology · 2016Article
- Signaling pathways in the molecular pathogenesis of adenocarcinomas of the esophagus and gastroesophageal junction.Cancer biology & therapy · 2013Review
- Diagnosis and management of Barrett's esophagus.The Surgical clinics of North America · 2012Review
- Math1/Atoh1 contributes to intestinalization of esophageal keratinocytes by inducing the expression of Muc2 and Keratin-20.Digestive diseases and sciences · 2012Article
- Molecular mechanisms of Barrett's esophagus.Digestive diseases and sciences · 2011Review
- NOTCH Signaling and ATOH1 in Colorectal Cancers.Current colorectal cancer reports · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundBarrett's esophagus (BE) is the predominant risk factor for the development of esophageal adenocarcinoma. BE is characterized by intestinal metaplasia with goblet cells. Reflux of bile acids is known to induce intestinal metaplasia, but the mechanisms are unclear. Inhibition of Notch signaling accompanied by increased Hath1 and induction of caudal homeobox 2 (CDX2) may be involved in development of intestinal goblet cells.
methodsEsophageal adenocarcinoma cell lines OE19 and OE33 were exposed for up to 8 hours to DCA (100-300 microM), and for up to 24 hours with and without the gamma-secretase inhibitor, DAPT (20 microM). Notch signaling components and CDX2 levels were measured by real-time PCR (for mRNA) and by Western blot analysis (for proteins).
resultsDCA induced a time and concentration dependent decrease in Notch pathway components mRNAs in OE33 and in the proteins in both cell lines. CDX2 mRNA and Hath1 protein were increased in OE19 by 3-fold. Inhibition of Notch pathway by DAPT decreased downstream Notch signaling mRNAs and proteins in both cell lines and increased Hath1 and CDX2 proteins only in OE19.
conclusionBile acid inhibition of Notch signaling in esophageal cells is correlated with an increase in Hath1 and CDX2 and may be one of the key processes contributing to the formation of BE.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.