Evidence map›Paper›PMID 17534574›Full record

ArticleJournal of human genetics2007

Association analysis of genetic variants in IL23R, ATG16L1 and 5p13.1 loci with Crohn's disease in Japanese patients.

Keiko Yamazaki, Yoshihiro Onouchi, Masakazu Takazoe, Michiaki Kubo, Yusuke Nakamura, Akira Hata

Open access · bronzeAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in Journal of human genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 13 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 13 pooled it
15.7field-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

75 citing papers in PubMed, 13 syntheses or guidelines pooled it, 206 citations in OpenAlex.

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  4. Genetic association between IL23R rs11209026 and rs10889677 polymorphisms and risk of Crohn's disease and ulcerative colitis: evidence from 41 studies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Pooled it
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  6. Association between ATG16L1 gene polymorphism and the risk of Crohn's disease.The Journal of international medical research · 2017
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  9. Interleukin-23 receptor genetic polymorphisms and Crohn's disease susceptibility: a meta-analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2010
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  20. Relationship between theInternational journal of environmental research and public health · 2019
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15 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Keiko YamazakiLaboratory for Gastrointestinal Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Kanagawa, Japan. kyama@src.riken.jp.
Yoshihiro OnouchiLaboratory for Gastrointestinal Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Kanagawa, Japan.
Masakazu TakazoeDepartment of Medicine, Division of Gastroenterology, Social Insurance Chuo General Hospital, Tokyo, Japan.
Michiaki KuboLaboratory for Genotyping, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Kanagawa, Japan.
Yusuke NakamuraLaboratory of Molecular Medicine, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Akira HataLaboratory for Gastrointestinal Diseases, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN), Kanagawa, Japan.
RIKEN · JPChiba University · JPThe University of Tokyo · JPTokyo Yamate Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel diseases, Crohn's disease (CD) and ulcerative colitis are characterised by chronic transmural, segmental and typically granulomatous inflammation of the gut. Each has a peak age of onset in the second to fourth decades of life and prevalence has been increasing significantly in both Western countries and Japan over the last decade, while their pathogenesis remains largely unknown. Recently, positive association of CD with the variants in interleukin 23 receptor (IL23R), autophagy-related 16-like 1 (ATG16L1) genes and chromosome 5p13.1 locus was reported through genome-wide association studies which are now recognised as a robust tool for the identification of susceptibility genes for complex diseases. To examine an association of reported susceptible variants in the three loci with Japanese CD patients, a total of 484 CD patients and 439 controls were genotyped. No evidence of positive association for any of these loci with CD was found in the Japanese population, even after clinically stratified subgroups of CD were used. Our result revealed a distinct ethnic difference of genetic background of CD that we reported previously in other genes between Japanese and Caucasian populations. Further genetic studies are required to confirm our findings with ethnically divergent populations.

Indexed as

Genetic VariationAdolescentAdultAgedAged, 80 and overAutophagy-Related ProteinsCarrier ProteinsCase-Control StudiesChildChromosomes, Human, Pair 5Crohn DiseaseFemaleGenetic MarkersGenetic Predisposition to DiseaseHumansJapanATG16L1 protein, humanAutophagy-Related ProteinsCarrier ProteinsGenetic MarkersIL23R protein, humanReceptors, Interleukin

Identifiers

PMID17534574
OpenAlexW2081521541

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.