ArticleBMC research notes2014
IL23R and ATG16L1 variants in Moroccan patients with inflammatory bowel disease.
Article in BMC research notes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 3 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 3 syntheses or guidelines pooled it, 13 citations in OpenAlex.
- Population stratified differences between ATG16L1 rs2241880 polymorphism with Crohn's disease risk: a systematic review and meta-analysis.BMC gastroenterology · 2025Pooled it
- Association between ATG16L1 gene polymorphism and the risk of Crohn's disease.The Journal of international medical research · 2017Pooled it
- Toll-like receptor 4 Asp299Gly and Thr399Ile polymorphisms: New data and a meta-analysis.BMC gastroenterology · 2014Pooled it
- Inflammatory bowel disease in Africa: what is the current state of knowledge?International health · 2020Review
- Harnessing the potential of gene editing technology using CRISPR in inflammatory bowel disease.World journal of gastroenterology · 2019Review
- Association between variants of the autophagy related gene ATG16L1 in inflammatory bowel diseases and clinical statues.Gastroenterology and hepatology from bed to bench · 2019Article
- Association of Autophagy Gene ATG16L1 Polymorphism with Human Prostate Cancer and Bladder Cancer in Turkish PopulationAsian Pacific journal of cancer prevention : APJCP · 2018Article
- CNTNAP3 associated ATG16L1 expression and Crohn's disease.Mediators of inflammation · 2015Article
- Association of inflammatory cytokine gene polymorphisms with inflammatory bowel disease in a Moroccan cohort.Genes and immunityArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInflammatory bowel diseases (IBD) are chronic diseases of the gastrointestinal tract. Although their pathogenesis is unclear, the combination of genetic predisposition and environmental components are believed to be the main cause of these diseases. Recently, many variants in interleukin 23 receptor (IL23R) and autophagy-related 16-like 1 (ATG16L1) genes have been associated with the disease. Our objective was to assess the frequency of ATG16L1 (T300A) and IL23R (L310P) variants in Moroccan IBD (Crohn's disease and Ulcerative Colitis) patients and to evaluate a possible effect of these variants on disease's phenotype and clinical course.
methods96 Moroccan IBD patients and 114 unrelated volunteers were genotyped for ATG16L1 (T300A) and IL23R (L310P) variants by PCR-restriction fragment length polymorphism.
resultsThis is the first report on the prevalence of ATG16L1 (T300A) and IL23R (L310P) variants in a Moroccan group. We found that IL23R (L310P) variant conferred a protective effect for crohn's disease (CD) but not ulcerative colitis (UC) patients. The presence of ATG16L1 (T300A) mutated alleles was associated with CD type but not with disease onset. In addition, the carriage of T300A variant alleles conferred a protective effect in UC.
conclusionOur results showed that the prevalence of ATG16L1 and IL23R variants was not significantly different between patients and controls. However a possible role of ATG16L1 (T300A) on CD phenotype was suggested.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.