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COX-1 polymorphism C50T, in complete linkage disequilibrium with the other polymorphism A-842G, has been depicted as a determinant of pharmacological response to aspirin treatment. Whether these polymorphisms exert an effect on response to aspirin both in vitro and ex vivo is still controversial. We genotyped a population of 148 healthy ...
A842G is located in the promoter of COX-1 and the Gallele creates a theoretic AP2 transcription factor site that might modify gene expression. The C50T encodes for a substitution (Pro17Leu) [6 ] amino acidsproximal to the signal peptide cleavage site, which may cause protein mis-compartmentalization. [5 ]
Analysis of four other polymorphisms, namely GPla (C807T), COX-1 (A842G/C50T), P2Y12 (H1/H2) and P2Y1 (A1622G), revealed no apparent association with aspirin resistance. However, the number of studies and of subjects used was small, making it difficult to exclude definitively any contribution of these polymorphisms to aspirin resistance.
This study was designed to investigate the association between the functional single-nucleotide polymorphism, A-842G/C50T, in the COX-1 gene and peptic ulcer bleeding. We obtained DNA samples from 106 patients who underwent upper gastrointestinal endoscopy because of bleeding peptic ulcer disease and from 88 healthy control subjects.
COX-1 polymorphism C50T, in complete linkage disequilibrium with the other polymorphism A-842G, has been depicted as a determinant of pharmacological response to aspirin treatment and it is found that there is no relationship between the 50T/-8 42G haplotype and the so-called phenomenon of aspirin resistance. Summary COX-1 polymorphism C50T, in complete linkage disequilibrium with the other ...
689 Pettinella et al. COX-1 polymorphisms C50T/A-842G and response to aspirin Discussion The incidence of the 50T allele of COX-1, equally distributed between males and females, was slightly lower (6.7% vs. >10% for heterozygosis and 0.67% vs. 1% for homozygosis) than previously reported in the Caucasian population (3, 4, 10).
The COX-1 A-842G/C50T SNP does not influence the risk for developing peptic ulcer bleeding. Discover the world's research. 25+ million members; ... for example, SNP of COX-1, A842G, and C50T.
Results: COX‐1 haplotype was significantly associated with aspirin response determined by AA‐induced platelet aggregation (P = 0.004; ... This haplotype carried by 12% of the population contains the minor allele of the promoter variant −A842G variant and is known to be in complete linkage disequilibrium with another variant, C50T in the ...
Of the non-responders detected by AA, 3 of 5 (60%) carried the rare G allele for the -A842G polymorphism of COX-1 in contrast to 16 of 96 (17%) responders (P = 0.016). Diabetes was associated with poor response. Aspirin non-response detected by PFA-100 associated with C13254T polymorphism of GP VI and female gender (P = 0.012 and P = 0.019 ...
The authors concluded that this functional SNP in the COX-1 locus may ultimately improve the safe and effective use of aspirin by better tailoring of dosage with an individual's genetic variation. 26 Most recently, Maree et al. 27 genotyped patients for five SNPs in COX-1: A842G, C22T (R8W), G128A (Q41Q), C644A (G213G), and C714A (L237M).