Evidence map›Paper›PMID 24376643›Full record

ArticlePloS one2013

Use of net reclassification improvement (NRI) method confirms the utility of combined genetic risk score to predict type 2 diabetes.

Claudia H T Tam, Janice S K Ho, Ying Wang, Vincent K L Lam, Heung Man Lee, Guozhi Jiang, Eric S H Lau, Alice P S Kong, Xiaodan Fan, Jean L F Woo and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 3 pooled it
4.2field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 3 syntheses or guidelines pooled it, 32 citations in OpenAlex.

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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

15 authors at 2 institutions in 2 countries.

Claudia H T TamDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China.
Janice S K HoDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China.
Ying WangDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China.
Vincent K L LamDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China.
Heung Man LeeDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China.
Guozhi JiangDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China.
Eric S H LauDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China.
Alice P S KongDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China ; Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong SAR, China ; Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China.
Xiaodan FanDepartment of Statistics, The Chinese University of Hong Kong, Hong Kong SAR, China.
Jean L F WooDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China.
Stephen K W TsuiSchool of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China.
Maggie C Y NgCenter for Genomics and Personalized Medicine Research, Center for Diabetes Research, Wake Forest School of Medicine, Winston-Salem, North Carolina, United States of America.
Wing Yee SoDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China ; Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong SAR, China ; Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China.
Juliana C N ChanDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China ; Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong SAR, China ; Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China.
Ronald C W MaDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong SAR, China ; Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Hong Kong SAR, China ; Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China.
Chinese University of Hong Kong · CNWake Forest University · US

Funding

Identifying variants causal for Type 2 Diabetes in Major human populationsU01DK085545 · NIDDK · UNIVERSITY OF OXFORD · PI CHAN, JULIANA CN, EBRAHIM, SHAH BRIAN · 2009 to 2013
$2.8M
NIDDK NIH HHS U01 DK085545
6 · The paper itself

Abstract

backgroundRecent genome-wide association studies (GWAS) identified more than 70 novel loci for type 2 diabetes (T2D), some of which have been widely replicated in Asian populations. In this study, we investigated their individual and combined effects on T2D in a Chinese population. METHODOLOGY: We selected 14 single nucleotide polymorphisms (SNPs) in T2D genes relating to beta-cell function validated in Asian populations and genotyped them in 5882 Chinese T2D patients and 2569 healthy controls. A combined genetic score (CGS) was calculated by summing up the number of risk alleles or weighted by the effect size for each SNP under an additive genetic model. We tested for associations by either logistic or linear regression analysis for T2D and quantitative traits, respectively. The contribution of the CGS for predicting T2D risk was evaluated by receiver operating characteristic (ROC) analysis and net reclassification improvement (NRI).

resultsWe observed consistent and significant associations of IGF2BP2, WFS1, CDKAL1, SLC30A8, CDKN2A/B, HHEX, TCF7L2 and KCNQ1 (8.5×10(-18)<P<8.5×10(-3)), as well as nominal associations of NOTCH2, JAZF1, KCNJ11 and HNF1B (0.05<P<0.1) with T2D risk, which yielded odds ratios ranging from 1.07 to 2.09. The 8 significant SNPs exhibited joint effect on increasing T2D risk, fasting plasma glucose and use of insulin therapy as well as reducing HOMA-β, BMI, waist circumference and younger age of diagnosis of T2D. The addition of CGS marginally increased AUC (2%) but significantly improved the predictive ability on T2D risk by 11.2% and 11.3% for unweighted and weighted CGS, respectively using the NRI approach (P<0.001).

conclusionIn a Chinese population, the use of a CGS of 8 SNPs modestly but significantly improved its discriminative ability to predict T2D above and beyond that attributed to clinical risk factors (sex, age and BMI).

Indexed as

AllelesGenetic Predisposition to DiseaseModels, GeneticPolymorphism, Single NucleotideAdultAgedAge FactorsAsian PeopleBlood GlucoseBody Mass IndexCase-Control StudiesDiabetes Mellitus, Type 2FemaleGene FrequencyGenome-Wide Association StudyHumansBlood Glucose

Identifiers

PMID24376643
PMCPMC3869744
OpenAlexW2104005244

What OpenQuestion holds

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LicenceCC BY
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.