Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2007-10-16
pubmed:abstractText
Bile reflux contributes to oesophageal injury and neoplasia. COX-2 is involved in both inflammation and carcinogenesis; however, the precise mechanisms by which bile acids promote COX-2 expression in the oesophagus are largely unknown. We analysed the molecular mechanisms that govern bile acid-mediated expression of COX-2 in Barrett's oesophagus and oesophageal adenocarcinoma (OA).
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1468-3288
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
56
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1512-21
pubmed:dateRevised
2010-11-2
pubmed:meshHeading
pubmed-meshheading:17604323-Adenocarcinoma, pubmed-meshheading:17604323-Animals, pubmed-meshheading:17604323-Barrett Esophagus, pubmed-meshheading:17604323-Bile Acids and Salts, pubmed-meshheading:17604323-CREB-Binding Protein, pubmed-meshheading:17604323-Cell Communication, pubmed-meshheading:17604323-Cell Transformation, Neoplastic, pubmed-meshheading:17604323-Cyclooxygenase 2, pubmed-meshheading:17604323-Esophageal Neoplasms, pubmed-meshheading:17604323-Gastroesophageal Reflux, pubmed-meshheading:17604323-Humans, pubmed-meshheading:17604323-Immunohistochemistry, pubmed-meshheading:17604323-Mitogen-Activated Protein Kinase 3, pubmed-meshheading:17604323-Rats, pubmed-meshheading:17604323-Rats, Sprague-Dawley, pubmed-meshheading:17604323-Reactive Oxygen Species, pubmed-meshheading:17604323-Tumor Cells, Cultured
pubmed:year
2007
pubmed:articleTitle
COX-2 induction by unconjugated bile acids involves reactive oxygen species-mediated signalling pathways in Barrett's oesophagus and oesophageal adenocarcinoma.
pubmed:affiliation
Department of Gastrointestinal Medicine and Nutrition, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030-4009, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural