Journals / Turkish Journal of Gastroenterology / 2016 / Cilt: 27 - Sayı: 6

Investigation of IL23R, JAK2, and STAT3 gene polymorphisms and gene-gene interactions in Crohn's disease and ulcerative colitis in a Turkish population

Pages
525–536
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

It was demonstrated that these polymorphisms may be effective in the etiology of inflammatory bowel disease in this Turkish population.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Background/Aims: Inflammatory bowel diseases are chronic, relapsing, inflammatory conditions.
📊
Key Findings & Data:The aim of our study is to investigate the involvement of IL23R, JAK2, and STAT3 polymorphisms in inflammatory bowel diseases in a Turkish population.Materials and Methods: Polymorphisms in IL23R (rs11209026), JAK2 (rs10758669), and STAT3 (rs3816769, rs2293152, rs744166, rs957970, rs8074524) were genotyped in 69 Crohn's disease patients, 157 ulcerative colitis patients, and 89 healthy controls.
💡
Conclusion & Impact:It was demonstrated that these polymorphisms may be effective in the etiology of inflammatory bowel disease in this Turkish population.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Özet

Background/Aims: Inflammatory bowel diseases are chronic, relapsing, inflammatory conditions. They have a genetic backround resulting in patient susceptibility. The aim of our study is to investigate the involvement of IL23R, JAK2, and STAT3 polymorphisms in inflammatory bowel diseases in a Turkish population.Materials and Methods: Polymorphisms in IL23R (rs11209026), JAK2 (rs10758669), and STAT3 (rs3816769, rs2293152, rs744166, rs957970, rs8074524) were genotyped in 69 Crohn's disease patients, 157 ulcerative colitis patients, and 89 healthy controls. Results: The presence of (C) in rs10758669, (T) and (TT) in rs957970, and (TT) in rs744166 were found to increase the susceptibility to Crohn's disease (p=0.049, p=0.016, p=0.010, p=0.035, respectively), while rs2293152 (GC), rs744166 (CT), and rs957970 (CT) provide protection against Crohn's disease (p=0.007, p=0.043, p=0.043, respectively). While rs2293152 (GC) was protective, rs2293152 (CC) increased the susceptibility to ulcerative colitis (p=0.009, p=0.001). All the polymorphisms were associated with age-at-diagnosis, except rs11209026. Furthermore, rs2293152 was associated with an extension in ulcerative colitis, while rs10758669, rs3816769, rs744166, rs2293152, and rs957970 were associated with the subphenotype in Crohn's disease. The presence of rs10758669 (AC) was protective against perianal Crohn's disease (p=0.016). Additionally, rs10758669 and rs2293152 in Crohn's disease and rs8074524, rs3816769, and rs10758669 in ulcerative colitis were associated with the requirement of immunsuppression. Finally, rs8074524 and rs10758669 in Crohn's disease and rs11209026 in ulcerative colitis were associated with disease-related operation. Conclusion: This is the first study of the single marker association of IL23R, JAK2, and STAT3 polymorphisms with ulcerative colitis and Crohn's disease in a Turkish population. It was demonstrated that these polymorphisms may be effective in the etiology of inflammatory bowel disease in this Turkish population.

🔖

Cite This Article

CAN, G., TEZEL, H. A., GÜRKAN, H., TOZKIR, H., ÜNSAL, G., SOYLU, A. R., ÜMİT, H. C. (2016). Investigation of IL23R, JAK2, and STAT3 gene polymorphisms and gene-gene interactions in Crohn's disease and ulcerative colitis in a Turkish population. Turkish Journal of Gastroenterology, Cilt: 27 - Sayı: 6, 525–536. https://ajindex.com/articles/411443

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (15)

  1. Loftus EV Jr. Clinical epidemiology of inflammatory bowel dis- ease: Incidence, prevalence, and environmental influences. Gas- troenterology 2004
  2. [CrossRef] Xavier RJ, Podolsky DK. Unravelling the pathogenesis of inflam- matory bowel disease. Nature 2007
  3. [CrossRef] Sartor RB. Mechanisms of disease: pathogenesis of Crohn's dis- ease and ulcerative colitis. Nat Clin Pract Gastroenterol Hepatol 2006
  4. [CrossRef] Zheng CQ, Hu GZ, Zeng ZS, Lin LJ, Gu GG. Progress in searching for susceptibility gene for inflammatory bowel disease by posi- tional cloning. World J Gastroenterol 2003
  5. [CrossRef] Wellcome Trust Case Control Consortium. Genome-wide associa- tion study of 14,000 cases of seven common diseases and 3,000 shared controls. Nature 2007
  6. [CrossRef] Barrett JC, Hansoul S, Nicolae DL, et al. Genome-wide association defines more than 30 distinct susceptibility loci for Crohn's dis- ease. Nat Genet 2008
  7. [CrossRef] Franke A, McGovern DP, Barrett JC, et al. Genome-wide meta- analysis increases to 71 the number of confirmed Crohn's disease susceptibility loci. Nat Genet 2010
  8. [CrossRef] Abraham C, Cho JH. Inflammatory bowel disease. N Engl J Med 2009
  9. [CrossRef] Duerr RH, Taylor KD, Brant SR, et al. A genome-wide association study identifies IL23R as an inflammatory bowel disease gene. Science 2006
  10. [CrossRef] Rioux JD, Xavier RJ, Taylor KD, et al. Genome-wide association study identifies new susceptibility loci for Crohn disease and im- plicates autophagy in disease pathogenesis. Nat Genet 2007
  11. [CrossRef] Wang K, Zhang H, Kugathasan S, et al. Diverse genome-wide as- sociation studies associate the IL12/IL23 pathway with Crohn Dis- ease. Am J Hum Genet 2009
  12. [CrossRef] Fisher SA, Tremelling M, Anderson CA, et al. Genetic determinants of ulcerative colitis include the ECM1 locus and five loci impli- cated in Crohn's disease. Nat Genet 2008
  13. [CrossRef] Franke A, Balschun T, Karlsen TH, et al. Replication of signals from recent studies of Crohn's disease identifies previously unknown disease loci for ulcerative colitis. Nat Genet 2008
  14. [CrossRef] Abraham C, Cho JH. IL-23 and autoimmunity: new insights into the pathogenesis of inflammatory bowel disease. Annu Rev Med 2009
  15. [CrossRef] Polgar N, Csongei V, Szabo M, et al. Investigation of JAK2, STAT3 and CCR6 polymorphisms and their gene-gene