Evidence map›Paper›PMID 17484864›Full record

ArticleGastroenterology2007

A nonsynonymous SNP in ATG16L1 predisposes to ileal Crohn's disease and is independent of CARD15 and IBD5.

Natalie J Prescott, Sheila A Fisher, Andre Franke, Jochen Hampe, Clive M Onnie, Dianne Soars, Richard Bagnall, Muddassar M Mirza, Jeremy Sanderson, Alastair Forbes and 4 more

Abstract read
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In one paragraph

Article in Gastroenterology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 7 pooled it
19.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

124 citing papers in PubMed, 7 syntheses or guidelines pooled it, 296 citations in OpenAlex.

  1. Pooled it
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  3. Association between ATG16L1 gene polymorphism and the risk of Crohn's disease.The Journal of international medical research · 2017
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  17. Saudi consensus guidance for the management of inflammatory bowel disease during pregnancy.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association · 2023
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64 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 6 institutions in 2 countries.

Natalie J PrescottDepartment of Medical and Molecular Genetics, King's College London School of Medicine, Guy's Hospital, London, UK.
Sheila A Fisher
Andre Franke
Jochen Hampe
Clive M Onnie
Dianne Soars
Richard Bagnall
Muddassar M Mirza
Jeremy Sanderson
Alastair Forbes
John C Mansfield
Cathryn M Lewis
Stefan Schreiber
Christopher G Mathew
Guy's Hospital · GBKing's College London · GBKiel University · DEGuy's and St Thomas' NHS Foundation Trust · GBNewcastle University · GBSt Mark's Hospital · GB

Funding

Medical Research Council G0000934Wellcome Trust 068545/Z/02
6 · The paper itself

Abstract

BACKGROUND &

aimsA genome-wide association scan of nonsynonymous DNA polymorphisms identified association of a threonine-to-alanine substitution (T300A) in the autophagy-related 16-like gene ATG16L1 with Crohn's disease. We investigated this association in independent U.K. cohorts of Crohn's disease and ulcerative colitis.

methodsThe T300A variant (rs2241880) was genotyped in an independent sample of 727 Crohn's disease and 877 ulcerative colitis cases, and in 579 controls. We then performed an extension analysis combining these data with the U.K. data from the initial study to give a total of 1236 U.K. Crohn's disease cases and 1235 controls to estimate disease risk and test for interaction with the CARD15 and IBD5 risk loci and for association with disease subtypes.

resultsThe association of T300A was replicated in the independent sample of 727 Crohn's disease cases (P = .001), and was strongly associated in the extended analysis of 1236 Crohn's cases (P = 2.4 x 10(-6)). The 300A/A genotype conferred a 1.65-fold risk of Crohn's disease, with a 2.2-fold risk of ileal disease. Analysis of the interaction of ATG16L1 with CARD15 and IBD5 indicated that all 3 loci contribute independently to disease risk. Homozygosity for the risk allele at all 3 loci conferred a combined risk of 20.4 (95% confidence interval: 8.71, 47.7) for Crohn's disease. The ATG16L1 risk genotype showed a modest but significant association with ulcerative colitis (P = .026).

conclusionsThe association of ATG16L1 with Crohn's disease and possibly with ulcerative colitis supports a role for autophagy in the pathogenesis of inflammatory bowel disease.

Indexed as

AdolescentAdultAgedAutophagyAutophagy-Related ProteinsCarrier ProteinsChildChild, PreschoolChromosomes, Human, Pair 5Cohort StudiesColitis, UlcerativeCrohn DiseaseEpistasis, GeneticFemaleGenetic Predisposition to DiseaseGenotypeATG16L1 protein, humanAutophagy-Related ProteinsCarrier ProteinsNOD2 protein, humanNod2 Signaling Adaptor Protein

Identifiers

PMID17484864
OpenAlexW2093356677

What OpenQuestion holds

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Registered trials

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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.