Evidence map›Paper›PMID 19956106›Full record

ArticleGenes and immunity2009

Analysis of 19 genes for association with type I diabetes in the Type I Diabetes Genetics Consortium families.

J M M Howson, N M Walker, D J Smyth, J A Todd, Type I Diabetes Genetics Consortium

Abstract read
In one paragraph

Article in Genes and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

42 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. International journal of molecular sciences · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Genetics: Is LADA just late onset type 1 diabetes?Frontiers in endocrinology · 2022
    Article
  11. Observational
  12. Influence ofFrontiers in immunology · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article
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

5 authors.

J M M HowsonJuvenile Diabetes Research Foundation/Wellcome Trust Diabetes and Inflammation Laboratory, Cambridge Institute for Medical Research, University of Cambridge, Addenbrooke's Hospital, Hills Road, Cambridge, UK. Joanna.Howson@cimr.cam.ac.uk
N M Walker
D J Smyth
J A Todd
Type I Diabetes Genetics Consortium

Funding

Type 1 Diabetes Genetics ConsortiumU01DK062418 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI RICH, STEPHEN S. · 2002 to 2007
$59.8M
AN NCRR CENTER FOR HIGH THROUGHPUT SNP GENOTYPING AND ANALYSIS: GAIN NETWORKU54RR020278 · NCRR · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI GABRIEL, STACEY · 2004 to 2008
$14.4M
British Heart Foundation RG/08/014/24067Medical Research Council G0000934NCRR NIH HHS U54 RR020278NIDDK NIH HHS U01 DK062418Wellcome Trust 061858Wellcome Trust 079895
6 · The paper itself

Abstract

In recent years the pace of discovery of genetic associations with type I diabetes (T1D) has accelerated, with the total number of confirmed loci, including the major histocompatibility complex (MHC) region, reaching 43. However, much of the deciphering of the associations at these, and the established T1D loci, has yet to be performed in sufficient numbers of samples or with sufficient markers. Here, 257 single-nucleotide polymorphisms (SNPs) have been genotyped in 19 candidate genes (INS, PTPN22, IL2RA, CTLA4, IFIH1, SUMO4, VDR, PAX4, OAS1, IRS1, IL4, IL4R, IL13, IL12B, CEACAM21, CAPSL, Q7Z4c4(5Q), FOXP3, EFHB) in 2300 affected sib-pair families and tested for association with T1D as part of the Type I Diabetes Genetics Consortium's candidate gene study. The study had approximately 80% power at alpha=0.002 and a minor allele frequency of 0.2 to detect an effect with a relative risk (RR) of 1.20, which drops to just 40% power for a RR of 1.15. At the INS gene, rs689 (-23 HphI) was the most associated SNP (P=3.8 x 10(-31)), with the estimated RR=0.57 (95% confidence interval, 0.52-0.63). In addition, rs689 was associated with age-at-diagnosis of T1D (P=0.001), with homozygosity for the T1D protective T allele, delaying the onset of T1D by approximately 2 years in these families. At PTPN22, rs2476601 (R620W), in agreement with previous reports, was the most significantly associated SNP (P=6.9 x 10(-17)), with RR=1.55 (1.40-1.72). Evidence for association with T1D was observed for the IFIH1 SNP, rs1990760 (P=7.0 x 10(-4)), with RR=0.88 (0.82-0.95) and the CTLA4 SNP rs1427676 (P=0.0005), with RR=1.14 (1.06-1.23). In contrast, no convincing evidence of association was obtained for SUMO4, VDR, PAX4, OAS1, IRS1, IL4, IL4R, IL13, IL12B, CEACAM21 or CAPSL gene regions (http://www.T1DBase.org).

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAllelesDiabetes Mellitus, Type 1FemaleGenotypeHumansMaleNuclear FamilyRisk Factors

Identifiers

PMID19956106
PMCPMC2810493

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.