Evidence map›Paper›PMID 32677173›Full record

ArticleGenetic epidemiology2020

Leveraging existing GWAS summary data of genetically correlated and uncorrelated traits to improve power for a new GWAS.

Haoran Xue, Chong Wu, Wei Pan

Open access · greenAbstract read
In one paragraph

Article in Genetic epidemiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 29% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. 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

3 authors at 2 institutions in 1 country.

Haoran XueSchool of Statistics, University of Minnesota, Minneapolis, Minnesota.
Chong WuDepartment of Statistics, Florida State University, Tallahassee, Florida.ORCID 0000-0002-8400-1785
Wei PanDivision of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, Minnesota.ORCID 0000-0002-1159-0582
University of Minnesota · USFlorida State University · US

Funding

Association analysis of rare variants with sequencing dataR01HL116720 · NHLBI · UNIVERSITY OF MINNESOTA · PI PAN, WEI, WEI, PENG · 2013 to 2020
$3.3M
Estimation and inference in directed acyclic graphical models for biological networksR01AG074858 · NIA · UNIVERSITY OF MINNESOTA · PI Wei Pan, XIAOTONG Tom SHEN · 2022 to 2026
$3.2M
Discovering causal genes, brain regions and other risk factors for Alzheimer's DiseaseR01AG065636 · NIA · UNIVERSITY OF MINNESOTA · PI PAN, WEI · 2020 to 2024
$3.1M
Powerful Inference and Prediction for Genetic AssociationR01HL105397 · NHLBI · UNIVERSITY OF MINNESOTA · PI PAN, WEI, SHEN, XIAOTONG TOM · 2011 to 2018
$2.9M
Estimation and Inference of Gene Regulatory NetworksR01GM126002 · NIGMS · UNIVERSITY OF MINNESOTA · PI PAN, WEI, SHEN, XIAOTONG TOM · 2017 to 2020
$1.4M
Statistical Methods for Genomic DataR01GM113250 · NIGMS · UNIVERSITY OF MINNESOTA · PI PAN, WEI · 2014 to 2017
$702k
Integrating genomic and imaging endophenotypes in GWASR21AG057038 · NIA · UNIVERSITY OF MINNESOTA · PI PAN, WEI · 2017 to 2018
$405k
NHLBI NIH HHS R01 HL105397NHLBI NIH HHS R01 HL116720NIA NIH HHS R01 AG065636NIA NIH HHS R01 AG074858NIA NIH HHS R21 AG057038NIGMS NIH HHS R01 GM113250NIGMS NIH HHS R01 GM126002
6 · The paper itself

Abstract

In spite of the tremendous success of genome-wide association studies (GWAS) in identifying genetic variants associated with complex traits and common diseases, many more are yet to be discovered. Hence, it is always desirable to improve the statistical power of GWAS. Paralleling with the intensive efforts of integrating GWAS with functional annotations or other omic data, we propose leveraging other published GWAS summary data to boost statistical power for a new/focus GWAS; the traits of the published GWAS may or may not be genetically correlated with the target trait of the new GWAS. Building on weighted hypothesis testing with a solid theoretical foundation, we develop a novel and effective method to construct single-nucleotide polymorphism (SNP)-specific weights based on 22 published GWAS data sets with various traits, detecting sometimes dramatically increased numbers of significant SNPs and independent loci as compared to the standard/unweighted analysis. For example, by integrating a schizophrenia GWAS summary data set with 19 other GWAS summary data sets of nonschizophrenia traits, our new method identified 1,585 genome-wide significant SNPs mapping to 15 linkage disequilibrium-independent loci, largely exceeding 818 significant SNPs in 13 independent loci identified by the standard/unweighted analysis; furthermore, using a later and larger schizophrenia GWAS summary data set as the validation data, 1,423 (out of 1,585) significant SNPs identified by the weighted analysis, compared to 705 (out of 818) by the unweighted analysis, were confirmed, while all 15 and 13 independent loci were also confirmed. Similar conclusions were reached with lipids and Alzheimer's disease (AD) traits. We conclude that the proposed approach is simple and cost-effective to improve GWAS power.

Indexed as

Alzheimer DiseaseGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansLinkage DisequilibriumLipidsMultifactorial InheritancePhenotypePolymorphism, Single NucleotideSchizophreniaLipidspleiotropySNPstatistical powerweighted hypothesis testing

Identifiers

PMID32677173
PMCPMC7722071
OpenAlexW3043554493

What OpenQuestion holds

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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.