ArticlePLoS genetics2012
A genome-wide scan of Ashkenazi Jewish Crohn's disease suggests novel susceptibility loci.
Article in PLoS genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 5 of them syntheses that pooled it.
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Who cites it
94 citing papers in PubMed, 5 syntheses or guidelines pooled it, 160 citations in OpenAlex.
- Position statement of the International Society for Gastrointestinal Hereditary Tumours (InSiGHT) onJournal of medical genetics · 2023Pooled it
- Trans-ancestry, Bayesian meta-analysis discovers 20 novel risk loci for inflammatory bowel disease in an African American, East Asian and European cohort.Human molecular genetics · 2023Pooled it
- Large-Scale Genome-Wide Association Study of East Asians Identifies Loci Associated With Risk for Colorectal Cancer.Gastroenterology · 2019Pooled it
- Genome-wide association study implicates immune activation of multiple integrin genes in inflammatory bowel disease.Nature genetics · 2017Pooled it
- Association of Interleukin-23 receptor gene polymorphisms with susceptibility to Crohn's disease: A meta-analysis.Scientific reports · 2015Pooled it
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- The chromatin and single-cell transcriptional landscapes of CD4 T cells in inflammatory bowel disease link risk loci with a proinflammatory Th17 cell population.Frontiers in immunology · 2023Article
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- A genome-wide association study in a large community-based cohort identifies multiple loci associated with susceptibility to bacterial and viral infections.Scientific reports · 2022Article
- Crohn's Disease Susceptibility and Onset Are Strongly Related to ThreeJournal of clinical medicine · 2021Article
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34 more citing papers are in PubMed but not listed here.
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Authors and funding
43 authors at 19 institutions in 3 countries.
Funding
Abstract
Crohn's disease (CD) is a complex disorder resulting from the interaction of intestinal microbiota with the host immune system in genetically susceptible individuals. The largest meta-analysis of genome-wide association to date identified 71 CD-susceptibility loci in individuals of European ancestry. An important epidemiological feature of CD is that it is 2-4 times more prevalent among individuals of Ashkenazi Jewish (AJ) descent compared to non-Jewish Europeans (NJ). To explore genetic variation associated with CD in AJs, we conducted a genome-wide association study (GWAS) by combining raw genotype data across 10 AJ cohorts consisting of 907 cases and 2,345 controls in the discovery stage, followed up by a replication study in 971 cases and 2,124 controls. We confirmed genome-wide significant associations of 9 known CD loci in AJs and replicated 3 additional loci with strong signal (p<5×10⁻⁶). Novel signals detected among AJs were mapped to chromosomes 5q21.1 (rs7705924, combined p = 2×10⁻⁸; combined odds ratio OR = 1.48), 2p15 (rs6545946, p = 7×10⁻⁹; OR = 1.16), 8q21.11 (rs12677663, p = 2×10⁻⁸; OR = 1.15), 10q26.3 (rs10734105, p = 3×10⁻⁸; OR = 1.27), and 11q12.1 (rs11229030, p = 8×10⁻⁹; OR = 1.15), implicating biologically plausible candidate genes, including RPL7, CPAMD8, PRG2, and PRG3. In all, the 16 replicated and newly discovered loci, in addition to the three coding NOD2 variants, accounted for 11.2% of the total genetic variance for CD risk in the AJ population. This study demonstrates the complementary value of genetic studies in the Ashkenazim.
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