ArticleBMC medical genetics2011
Evaluation of 22 genetic variants with Crohn's disease risk in the Ashkenazi Jewish population: a case-control study.
Article in BMC medical genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 7 of them syntheses that pooled it.
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Who cites it
30 citing papers in PubMed, 7 syntheses or guidelines pooled it, 47 citations in OpenAlex.
- ATG16L1 rs2241880/T300A increases susceptibility to perianal Crohn's disease: An updated meta-analysis on inflammatory bowel disease risk and clinical outcomes.United European gastroenterology journal · 2024Pooled it
- Association between PTGER4 polymorphisms and inflammatory bowel disease risk in Caucasian: A meta-analysis.Medicine · 2020Pooled it
- Association of Interleukin-23 receptor gene polymorphisms with susceptibility to Crohn's disease: A meta-analysis.Scientific reports · 2015Pooled it
- Contribution of NKX2-3 polymorphisms to inflammatory bowel diseases: a meta-analysis of 35358 subjects.Scientific reports · 2014Pooled it
- Associations between STAT3 rs744166 polymorphisms and susceptibility to ulcerative colitis and Crohn's disease: a meta-analysis.PloS one · 2014Pooled it
- Associations between PTPN2 polymorphisms and susceptibility to ulcerative colitis and Crohn's disease: a meta-analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Pooled it
- Pooled it
- Functional variants in theScience translational medicine · 2018Article
- Protein Tyrosine Phosphatases: Regulators of CD4 T Cells in Inflammatory Bowel Disease.Frontiers in immunology · 2018Review
- Association between genetic polymorphisms in the autophagy-related 5 gene promoter and the risk of sepsis.Scientific reports · 2017Article
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- Article
- Common NOD2/CARD15 and TLR4 Polymorphisms Are Associated with Crohn's Disease Phenotypes in Southeastern Brazilians.Digestive diseases and sciences · 2016Article
- Interaction between STAT3 gene polymorphisms and smoking on Crohn's disease susceptibility: a case-control study in a Chinese Han population.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016Article
- Effect of postnatal low-dose exposure to environmental chemicals on the gut microbiome in a rodent model.Microbiome · 2016Article
- PTGER4 gene variant rs76523431 is a candidate risk factor for radiological joint damage in rheumatoid arthritis patients: a genetic study of six cohorts.Arthritis research & therapy · 2015Article
- The TNF-family cytokine TL1A: from lymphocyte costimulator to disease co-conspirator.Journal of leukocyte biology · 2015Review
- Article
- PTGER4 modulating variants in Crohn's disease.International journal of colorectal disease · 2014Article
- Detection of Mycobacterium avium subspecies paratuberculosis in patients with Crohn's disease is unrelated to the presence of single nucleotide polymorphisms rs2241880 (ATG16L1) and rs10045431 (IL12B).Medical microbiology and immunology · 2014Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundCrohn's disease (CD) has the highest prevalence among individuals of Ashkenazi Jewish (AJ) descent compared to non-Jewish Caucasian populations (NJ). We evaluated a set of well-established CD-susceptibility variants to determine if they can explain the increased CD risk in the AJ population.
methodsWe recruited 369 AJ CD patients and 503 AJ controls, genotyped 22 single nucleotide polymorphisms (SNPs) at or near 10 CD-associated genes, NOD2, IL23R, IRGM, ATG16L1, PTGER4, NKX2-3, IL12B, PTPN2, TNFSF15 and STAT3, and assessed their association with CD status. We generated genetic scores based on the risk allele count alone and the risk allele count weighed by the effect size, and evaluated their predictive value.
resultsThree NOD2 SNPs, two IL23R SNPs, and one SNP each at IRGM and PTGER4 were independently associated with CD risk. Carriage of 7 or more copies of these risk alleles or the weighted genetic risk score of 7 or greater correctly classified 92% (allelic count score) and 83% (weighted score) of the controls; however, only 29% and 47% of the cases were identified as having the disease, respectively. This cutoff was associated with a >4-fold increased disease risk (p < 10e-16).
conclusionsCD-associated genetic risks were similar to those reported in NJ population and are unlikely to explain the excess prevalence of the disease in AJ individuals. These results support the existence of novel, yet unidentified, genetic variants unique to this population. Understanding of ethnic and racial differences in disease susceptibility may help unravel the pathogenesis of CD leading to new personalized diagnostic and therapeutic approaches.
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