Deoxycholic acid causes DNA damage while inducing apoptotic resistance through NF-κB activation in benign Barrett's epithelial cells. - Wikidata - wikimedia - TriplyDB

Deoxycholic acid causes DNA damage while inducing apoptotic resistance through NF-κB activation in benign Barrett's epithelial cells.

Deoxycholic acid causes DNA damage while inducing apoptotic resistance through NF-κB activation in benign Barrett's epithelial cells.

http://www.wikidata.org/entity/Q35159625

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Update on management of Barrett's esophagus Cross-talk between bile acids and gastrointestinal tract for progression and development of cancer and its therapeutic implications Nuclear factor kappa B role in inflammation associated gastrointestinal malignancies Barrett's esophagus in 2012: updates in pathogenesis, treatment, and surveillance Signaling pathways in the molecular pathogenesis of adenocarcinomas of the esophagus and gastroesophageal junction Abdominal obesity and gastroesophageal cancer risk: systematic review and meta-analysis of prospective studies Glutathione Peroxidase 7 Suppresses Bile Salt-Induced Expression of Pro-Inflammatory Cytokines in Barrett's Carcinogenesis.Loss of glutathione peroxidase 7 promotes TNF-α-induced NF-κB activation in Barrett's carcinogenesis.In Barrett's esophagus patients and Barrett's cell lines, ursodeoxycholic acid increases antioxidant expression and prevents DNA damage by bile acids.Bile acid dysregulation, gut dysbiosis, and gastrointestinal cancer.Pathophysiological mechanisms linking obesity and esophageal adenocarcinoma Proinflammatory cytokines and bile acids upregulate ΔNp73 protein, an inhibitor of p53 and p73 tumor suppressors.Review: Experimental models for Barrett's esophagus and esophageal adenocarcinoma Barrett esophagus: history, definition and etiopathogeny Proton Pump Inhibitors Do Not Reduce the Risk of Esophageal Adenocarcinoma in Patients with Barrett's Esophagus: A Systematic Review and Meta-Analysis.Targeting the intrinsic inflammatory pathway: honokiol exerts proapoptotic effects through STAT3 inhibition in transformed Barrett's cells.Inhibition of NF-κB by deoxycholic acid induces miR-21/PDCD4-dependent hepatocelular apoptosis.Comparison of Cytotoxic Activity of Bile on HepG2 and CCRF-CEM Cell Lines: An in Vitro Study.Gastro-duodenal fluid induced nuclear factor-κappaB activation and early pre-malignant alterations in murine hypopharyngeal mucosa Clinical Study of Ursodeoxycholic Acid in Barrett's Esophagus Patients.From Reflux Esophagitis to Esophageal Adenocarcinoma.APE1-mediated DNA damage repair provides survival advantage for esophageal adenocarcinoma cells in response to acidic bile salts.1,25-dihydroxyvitamin D in the pathogenesis of Barrett's esophagus and esophageal adenocarcinoma.Cellular origins and molecular mechanisms of Barrett's esophagus and esophageal adenocarcinoma.Proton Pump Inhibitors: The Culprit for Barrett's Esophagus?Mechanisms of Barrett's oesophagus: intestinal differentiation, stem cells, and tissue models.Activation of NADPH oxidases leads to DNA damage in esophageal cells.A 4-Phenoxyphenol Derivative Exerts Inhibitory Effects on Human Hepatocellular Carcinoma Cells through Regulating Autophagy and Apoptosis Accompanied by Downregulating α-Tubulin Expression.Barrett's metaplasia develops from cellular reprograming of esophageal squamous epithelium due to gastroesophageal reflux.Prevention of DNA damage in Barrett's esophageal cells exposed to acidic bile salts.In vitro model for gastroduodenal reflux-induced nuclear factor-kappaB activation and its role in hypopharyngeal carcinogenesis.Reflux composition influences the level of NF-κB activation and upstream kinase preference in oesophageal adenocarcinoma cells.Adiponectin modulates DCA-induced inflammation via the ROS/NF-κ B signaling pathway in esophageal adenocarcinoma cells.Prolonged exposure to acid and bile induces chromosome abnormalities that precede malignant transformation of benign Barrett's epithelium.Optimizing the diagnosis and therapy of Barrett's esophagus.A weakly acidic solution containing deoxycholic acid induces esophageal epithelial apoptosis and impairs integrity in an in vivo perfusion rabbit model.Intrinsic resistance triggered under acid loading within normal esophageal epithelial cells: NHE1- and ROS-mediated survival.Bile acid receptor TGR5, NADPH Oxidase NOX5-S and CREB Mediate Bile Acid-Induced DNA Damage In Barrett's Esophageal Adenocarcinoma Cells.Bile acid and cigarette smoke enhance the aggressive phenotype of esophageal adenocarcinoma cells by downregulation of the mitochondrial uncoupling protein-2.Diallyl Disulfide Suppresses the Inflammation and Apoptosis Resistance Induced by DCA Through ROS and the NF-κB Signaling Pathway in Human Barrett's Epithelial Cells.

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P2860

Deoxycholic acid causes DNA damage while inducing apoptotic resistance through NF-κB activation in benign Barrett's epithelial cells.

http://www.wikidata.org/entity/Q35159625

description

2011 nî lūn-bûn

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2011 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2011 թվականի հունիսին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Deoxycholic acid causes DNA da ...... gn Barrett's epithelial cells.

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Deoxycholic acid causes DNA da ...... gn Barrett's epithelial cells.

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type

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Deoxycholic acid causes DNA da ...... gn Barrett's epithelial cells.

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Deoxycholic acid causes DNA da ...... gn Barrett's epithelial cells.

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Deoxycholic acid causes DNA da ...... gn Barrett's epithelial cells.

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Deoxycholic acid causes DNA da ...... gn Barrett's epithelial cells.

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AJPGI.00092.2011

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American Journal of Physiology - Gastrointestinal and Liver Physiology

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Deoxycholic acid causes DNA da ...... gn Barrett's epithelial cells.

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Chunhua Yu

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David H Wang

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Davood Rezaei

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Edaire Cheng

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Eric D Strauch

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Frank Meyer

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Jian-Ying Wang

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Qiuyang Zhang

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Rhonda F Souza

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Stefanie Juergens

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P2860

The Hallmarks of Cancer

Ursodeoxycholic acid therapy in hepatobiliary disease

Malignant transformation of non-neoplastic Barrett's epithelial cells through well-defined genetic manipulations

GammaH2AX and cancer

Induction of H2AX phosphorylation in pulmonary cells by tobacco smoke: a new assay for carcinogens.

Ursodiol use is associated with lower prevalence of colonic neoplasia in patients with ulcerative colitis and primary sclerosing cholangitis.

History, molecular mechanisms, and endoscopic treatment of Barrett's esophagus.

Acid and bile salt-induced CDX2 expression differs in esophageal squamous cells from patients with and without Barrett's esophagus.

Putative telomere-independent mechanisms of replicative aging reflect inadequate growth conditions.

The role of DNA breaks in genomic instability and tumorigenesis.

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10.1152/AJPGI.00092.2011

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21636532

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apoptotic process

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