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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
2006-4-18
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pubmed:abstractText |
Although progression to adenocarcinoma at the gastroesophageal junction reflects exposure to acid and bile acids associated with reflux, mechanisms mediating this transformation remain undefined. Guanylyl cyclase C (GC-C), an intestine-specific tumor suppressor, may represent a mechanism-based marker and target of transformation at the gastroesophageal junction. The present studies examine the expression of GC-C in normal tissues and tumors from esophagus and stomach and mechanisms regulating its expression by acid and bile acids.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Bile Acids and Salts,
http://linkedlifedata.com/resource/pubmed/chemical/CDX2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Deoxycholic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Guanylate Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/Homeodomain Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Guanylate Cyclase-Coupled,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Peptide,
http://linkedlifedata.com/resource/pubmed/chemical/enterotoxin receptor
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0016-5085
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pubmed:author |
pubmed-author:BirbeRuthR,
pubmed-author:ChervonevaInnaI,
pubmed-author:DebruynePhilip RPR,
pubmed-author:Domon-CellClaireC,
pubmed-author:FreundJean-NoelJN,
pubmed-author:JinTianruT,
pubmed-author:LiGongG,
pubmed-author:LiPengP,
pubmed-author:PalazzoJuan PJP,
pubmed-author:PitariGiovanni MGM,
pubmed-author:SchulzStephanieS,
pubmed-author:WaldmanScott ASA,
pubmed-author:WitekMatthewM
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pubmed:issnType |
Print
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pubmed:volume |
130
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1191-206
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:16618413-Adenocarcinoma,
pubmed-meshheading:16618413-Bile Acids and Salts,
pubmed-meshheading:16618413-Cell Line, Tumor,
pubmed-meshheading:16618413-Cell Transformation, Neoplastic,
pubmed-meshheading:16618413-Deoxycholic Acid,
pubmed-meshheading:16618413-Esophageal Neoplasms,
pubmed-meshheading:16618413-Esophagogastric Junction,
pubmed-meshheading:16618413-Esophagus,
pubmed-meshheading:16618413-Gene Expression,
pubmed-meshheading:16618413-Guanylate Cyclase,
pubmed-meshheading:16618413-Homeodomain Proteins,
pubmed-meshheading:16618413-Humans,
pubmed-meshheading:16618413-Intestines,
pubmed-meshheading:16618413-NF-kappa B,
pubmed-meshheading:16618413-Promoter Regions, Genetic,
pubmed-meshheading:16618413-RNA, Messenger,
pubmed-meshheading:16618413-Receptors, Guanylate Cyclase-Coupled,
pubmed-meshheading:16618413-Receptors, Peptide,
pubmed-meshheading:16618413-Tissue Distribution,
pubmed-meshheading:16618413-Transcription, Genetic
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pubmed:year |
2006
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pubmed:articleTitle |
Bile acids induce ectopic expression of intestinal guanylyl cyclase C Through nuclear factor-kappaB and Cdx2 in human esophageal cells.
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pubmed:affiliation |
Department of Pharmacology and Experimental Therapeutics, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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