ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2011
Deoxycholic acid causes DNA damage while inducing apoptotic resistance through NF-κB activation in benign Barrett's epithelial cells.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00858858 (Clinical Studies on Bile Acids in Barrett's Esophagus), which is not on this map. Cited by 68 papers, 3 of them syntheses that pooled it.
What it found
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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.
Clinical Studies on Bile Acids in Barrett's Esophagus
Who cites it
68 citing papers in PubMed, 3 syntheses or guidelines pooled it, 132 citations in OpenAlex.
- Abdominal obesity and gastroesophageal cancer risk: systematic review and meta-analysis of prospective studies.Bioscience reports · 2017Pooled it
- Pooled it
- Cell culture models for studying the development of Barrett's esophagus: a systematic review.Cellular oncology (Dordrecht, Netherlands) · 2012Pooled it
- Clinical Study of Ursodeoxycholic Acid in Barrett's Esophagus Patients.Cancer prevention research (Philadelphia, Pa.) · 2016Trial
- In Barrett's esophagus patients and Barrett's cell lines, ursodeoxycholic acid increases antioxidant expression and prevents DNA damage by bile acids.American journal of physiology. Gastrointestinal and liver physiology · 2014Trial
- Gut microbiota-derived metabolites as context-dependent modulators of Nrf2 signaling in inflammation-driven carcinogenesis.Gut microbes · 2026Review
- Beyond estrobolome 1.0: unraveling endocrine-microbiome axis as a driver and therapeutic target in hormone-driven cancers.NPJ biofilms and microbiomes · 2026Review
- 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
- Listening to the Past, Shaping the Future: A Data-mining Based and Visual Analysis of Five Decades of Gastric Carcinogenesis Research.Biological procedures online · 2025Article
- Antimicrobial and healing efficacy of bile salts with insights into cytotoxic activity.Scientific reports · 2025Article
- Increased reflux secondary bile acids are associated with changes to the microbiome and transcriptome in Barrett's esophagus.Gut microbes · 2025Article
- Multifaceted roles of microbiota-derived deoxycholic acid in gastrointestinal cancers: from barrier disruption to therapeutic implications.Human cell · 2025Review
- The role of the esophageal and intestinal microbiome in gastroesophageal reflux disease: past, present, and future.Frontiers in immunology · 2025Review
- Untargeted metabolomics for acute intra-abdominal infection diagnosis in serum and urine using UHPLC-TripleTOF MS.Frontiers in molecular biosciences · 2025Article
- Critical role of the gut microbiota in immune responses and cancer immunotherapy.Journal of hematology & oncology · 2024Review
- Role of the Microbiota in Skin Neoplasms: New Therapeutic Horizons.Microorganisms · 2023Review
- Article
- Bile acid sequestrants in poor healing after endoscopic therapy of Barrett's esophagus.Clinical endoscopy · 2023Article
- Seeking to understand non-responders to ablative therapy for dysplastic Barrett's esophagus.Clinical endoscopy · 2023Article
- Protein adduction causes non-mutational inhibition of p53 tumor suppressor.Cell reports · 2023Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
Abstract
Gastroesophageal reflux is associated with adenocarcinoma in Barrett's esophagus, but the incidence of this tumor is rising, despite widespread use of acid-suppressing medications. This suggests that refluxed material other than acid might contribute to carcinogenesis. We looked for potentially carcinogenetic effects of two bile acids, deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA), on Barrett's epithelial cells in vitro and in vivo. We exposed Barrett's (BAR-T) cells to DCA or UDCA and studied the generation of reactive oxygen/nitrogen species (ROS/RNS); expression of phosphorylated H2AX (a marker of DNA damage), phosphorylated IkBα, and phosphorylated p65 (activated NF-κB pathway proteins); and apoptosis. During endoscopy in patients, we took biopsy specimens of Barrett's mucosa before and after esophageal perfusion with DCA or UDCA and assessed DNA damage and NF-κB activation. Exposure to DCA, but not UDCA, resulted in ROS/RNS production, DNA damage, and NF-κB activation but did not increase the rate of apoptosis in BAR-T cells. Pretreatment with N-acetyl-l-cysteine (a ROS scavenger) prevented DNA damage after DCA exposure, and DCA did induce apoptosis in cells treated with NF-κB inhibitors (BAY 11-7085 or AdIκB superrepressor). DNA damage and NF-κB activation were detected in biopsy specimens of Barrett's mucosa taken after esophageal perfusion with DCA, but not UDCA. These data show that, in Barrett's epithelial cells, DCA induces ROS/RNS production, which causes genotoxic injury, and simultaneously induces activation of the NF-κB pathway, which enables cells with DNA damage to resist apoptosis. We have demonstrated molecular mechanisms whereby bile reflux might contribute to carcinogenesis in Barrett's esophagus.
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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.