Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-3-15
pubmed:abstractText
Prostaglandin H synthase 2 (PTGS2) or cyclooxygenase-2 (COX-2) has been shown to play a key role in the regulation of inflammation, and its inhibition is associated with a reduced risk of colon cancer. The PTGS2 (COX-2) -765G > C promoter variant is located in a putative SP1 binding site and reduces PTGS2 expression. In a Minnesota-based case-control study of cases with adenomatous (n = 494) or hyperplastic polyps (n = 186) versus polyp-free controls (n = 584), we investigated the role of the PTGS2 -765G > C promoter polymorphism. Multiple logistic regression analysis was used, adjusting for age, body mass index, caloric intake, alcohol, fiber, sex, hormone use, and smoking. For colorectal adenoma, odds ratios (OR) compared with PTGS2 -765GG as reference were GC 1.00 [95% confidence interval (95% CI), 0.74-1.35] and CC 0.53 (95% CI, 0.22-1.28). For hyperplastic polyps, the comparable adjusted odds ratios were GC 0.97 (95% CI, 0.65-1.46) and CC 0.24 (95% CI, 0.05-1.11). Risk associated with the -765G > C variant differed by aspirin or other nonsteroidal anti-inflammatory drug (NSAID) use. Among nonusers of aspirin or other NSAIDs, the CC genotype conferred a significant decrease in risk of adenoma (OR, 0.26; 95% CI, 0.07-0.89). Use of aspirin or other NSAIDs reduced risk of adenoma only among those with the -765GG (wild type) and possibly -765CG genotypes (OR, 0.66; 95% CI, 0.48-0.92 and OR, 0.64; 95% CI, 0.40-1.02, respectively). These data suggest that COX-2 expression or activity may be beneficially suppressed, and risk of colorectal polyps reduced, by aspirin or other NSAIDs in PTGS2 -765GG (wild type) individuals and by the -765 CC variant genotype in nonusers of NSAIDs.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1055-9965
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
616-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:15767339-Adenoma, pubmed-meshheading:15767339-Adult, pubmed-meshheading:15767339-Aged, pubmed-meshheading:15767339-Anti-Inflammatory Agents, Non-Steroidal, pubmed-meshheading:15767339-Case-Control Studies, pubmed-meshheading:15767339-Colorectal Neoplasms, pubmed-meshheading:15767339-Cyclooxygenase 2, pubmed-meshheading:15767339-Female, pubmed-meshheading:15767339-Humans, pubmed-meshheading:15767339-Inflammation, pubmed-meshheading:15767339-Male, pubmed-meshheading:15767339-Membrane Proteins, pubmed-meshheading:15767339-Middle Aged, pubmed-meshheading:15767339-Odds Ratio, pubmed-meshheading:15767339-Peroxidases, pubmed-meshheading:15767339-Polymorphism, Genetic, pubmed-meshheading:15767339-Promoter Regions, Genetic, pubmed-meshheading:15767339-Prostaglandin-Endoperoxide Synthases, pubmed-meshheading:15767339-Risk Factors
pubmed:year
2005
pubmed:articleTitle
PTGS2 (COX-2) -765G > C promoter variant reduces risk of colorectal adenoma among nonusers of nonsteroidal anti-inflammatory drugs.
pubmed:affiliation
Fred Hutchinson Cancer Research Center, Seattle, WA 98109-1024, USA. nulrich@fhcrc.org
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, N.I.H., Extramural