Linked Life Data

17023971

Source:http://linkedlifedata.com/resource/pubmed/id/17023971

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-10-6
pubmed:abstractText
Intestinal metaplasia in Barrett's esophagus is a major risk factor for esophageal adenocarcinoma, a tumor whose incidence rate has more than tripled in the United States over the past 2 decades. Studies have identified a number of molecular abnormalities that may be involved in the progression from dysplasia to cancer in Barrett's esophagus, including altered expression of cadherins and catenins; inactivation of tumor-suppressor genes, such as p53, p21, p27, and p16; and increased activity of the enzymes cyclooxygenase-2 and inducible nitric oxide synthase. Studies on the role of Helicobacter pylori in the pathogenesis of intestinal metaplasia at the gastroesophageal junction have yielded contradictory results. It appears, however, that gastric infection with strains of H. pylori containing a cagA gene associated with cytotoxin expression may protect against the development of dysplasia and adenocarcinoma in Barrett's esophagus. The role of ablation therapy for Barrett's esophagus remains controversial, largely because thermal and photochemical ablative techniques often leave foci of intestinal metaplasia behind.
pubmed:language
eng
pubmed:journal
pubmed:status
PubMed-not-MEDLINE
pubmed:month
Jul
pubmed:issn
0267-1379
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
352-8
pubmed:year
1999
pubmed:articleTitle
Barrett's esophagus.
pubmed:affiliation
Department of Veterans Affairs Medical Center, Dallas, Texas 75216, USA.
pubmed:publicationType
Journal Article