Association study between TRIM26 polymorphisms and risk of aspirin-exacerbated respiratory disease
- Authors
- Lee, Jin Sol; Bae, Joon Seol; Kim, Jeong-Hyun; Kim, Jason Yongha; Park, Tae Joon; Pasaje, Charisse Flerida; Park, Byung-Lae; Cheong, Hyun Sub; Jang, An-Soo; Uh, Soo-Taek; Park, Choon-Sik; Shin, Hyoung Doo
- Issue Date
- May-2012
- Publisher
- Demetrios A. Spandidos Ed. & Pub.
- Keywords
- aspirin-exacerbated respiratory disease; aspirin-tolerant asthma; tripartite motif-containing 26; polymorphisms; haplotypes
- Citation
- International Journal of Molecular Medicine, v.29, no.5, pp 927 - 933
- Pages
- 7
- Journal Title
- International Journal of Molecular Medicine
- Volume
- 29
- Number
- 5
- Start Page
- 927
- End Page
- 933
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/15240
- DOI
- 10.3892/ijmm.2012.898
- ISSN
- 1107-3756
1791-244X
- Abstract
- Aspirin-exacerbated respiratory disease (AERD) is a clinical syndrome that is characterized by nasal polyposis, general symptoms of asthma and sensitive response to nonsteroidal anti-inflammatory drugs (NSAIDs). Although the exact function of tripartite motif-containing 26 (TRIM26) still remains unknown, the gene functions in the immune response. Thus, we hypothesized that TRIM26 polymorphisms may affect aspirin-induced bronchospasm and explored whether the gene can be a marker for diagnosis of AERD. To investigate our hypothesis that TRIM26 may serve as a genetic marker for diagnosis of AERD), this study focused on demonstrating the associations between single nucleotide polymorphisms (SNPs) of the TRIM26 gene and AERD. We genotyped 18 polymorphisms of TRIM26 in a total of 189 asthmatics and examined their associations with the risk of AERD. We performed logistic analysis for obtaining P-values and regression analysis for demonstrating an association between the phenotype with FEV1 and the genotype. We observed no associations between polymorphisms in TRIM26 and the risk of AERD in both logistic and regression analyses. Although our results reveal a lack of association, the suggested functional role of TRIM26 makes it a putative candidate gene for AERD. Thus, replications in other populations using larger samples may provide valuable information for AERD etiology.
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