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@ARTICLE{Su:132947,
author = {Y.-R. Su and C. Di and S. Bien and L. Huang and X. Dong and
G. Abecasis and S. Berndt and S. Bezieau and H. Brenner$^*$
and B. Caan and G. Casey and J. Chang-Claude$^*$ and S.
Chanock and S. Chen and C. Connolly and K. Curtis and J.
Figueiredo and M. Gala and S. Gallinger and T. Harrison and
M. Hoffmeister$^*$ and J. Hopper and J. R. Huyghe and M.
Jenkins and A. Joshi and L. Le Marchand and P. Newcomb and
D. Nickerson and J. Potter and R. Schoen and M. Slattery and
E. White and B. Zanke and U. Peters and L. Hsu},
title = {{A} {M}ixed-{E}ffects {M}odel for {P}owerful {A}ssociation
{T}ests in {I}ntegrative {F}unctional {G}enomics.},
journal = {The American journal of human genetics},
volume = {102},
number = {5},
issn = {0002-9297},
address = {New York, NY [u.a.]},
publisher = {Cell Press},
reportid = {DKFZ-2018-00586},
pages = {904 - 919},
year = {2018},
abstract = {Genome-wide association studies (GWASs) have successfully
identified thousands of genetic variants for many complex
diseases; however, these variants explain only a small
fraction of the heritability. Recently, genetic association
studies that leverage external transcriptome data have
received much attention and shown promise for discovering
novel variants. One such approach, PrediXcan, is to use
predicted gene expression through genetic regulation.
However, there are limitations in this approach. The
predicted gene expression may be biased, resulting from
regularized regression applied to moderately sample-sized
reference studies. Further, some variants can individually
influence disease risk through alternative functional
mechanisms besides expression. Thus, testing only the
association of predicted gene expression as proposed in
PrediXcan will potentially lose power. To tackle these
challenges, we consider a unified mixed effects model that
formulates the association of intermediate phenotypes such
as imputed gene expression through fixed effects, while
allowing residual effects of individual variants to be
random. We consider a set-based score testing framework,
MiST (mixed effects score test), and propose two data-driven
combination approaches to jointly test for the fixed and
random effects. We establish the asymptotic distributions,
which enable rapid calculation of p values for genome-wide
analyses, and provide p values for fixed and random effects
separately to enhance interpretability over GWASs. Extensive
simulations demonstrate that our approaches are more
powerful than existing ones. We apply our approach to a
large-scale GWAS of colorectal cancer and identify two
genes, POU5F1B and ATF1, which would have otherwise been
missed by PrediXcan, after adjusting for all known loci.},
cin = {C070 / G110 / C020},
ddc = {570},
cid = {I:(DE-He78)C070-20160331 / I:(DE-He78)G110-20160331 /
I:(DE-He78)C020-20160331},
pnm = {313 - Cancer risk factors and prevention (POF3-313)},
pid = {G:(DE-HGF)POF3-313},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:29727690},
doi = {10.1016/j.ajhg.2018.03.019},
url = {https://inrepo02.dkfz.de/record/132947},
}