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GWAS Study

Heritability and genome-wide association study of benign prostatic hyperplasia (BPH) in the eMERGE network.

Hellwege JN, Stallings S, Torstenson ES et al.

30988330 PubMed ID
GWAS Study Type
10419 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

HJ
Hellwege JN
SS
Stallings S
TE
Torstenson ES
CR
Carroll R
BK
Borthwick KM
BM
Brilliant MH
CD
Crosslin D
GA
Gordon A
HG
Hripcsak G
JG
Jarvik GP
LJ
Linneman JG
DP
Devi P
PP
Peissig PL
SP
Sleiman PAM
HH
Hakonarson H
RM
Ritchie MD
VS
Verma SS
SN
Shang N
DJ
Denny JC
RD
Roden DM
VE
Velez Edwards DR
ET
Edwards TL
Chapter II

Abstract

Summary of the research findings

Benign prostatic hyperplasia (BPH) results in a significant public health burden due to the morbidity caused by the disease and many of the available remedies. As much as 70% of men over 70 will develop BPH. Few studies have been conducted to discover the genetic determinants of BPH risk. Understanding the biological basis for this condition may provide necessary insight for development of novel pharmaceutical therapies or risk prediction. We have evaluated SNP-based heritability of BPH in two cohorts and conducted a genome-wide association study (GWAS) of BPH risk using 2,656 cases and 7,763 controls identified from the Electronic Medical Records and Genomics (eMERGE) network. SNP-based heritability estimates suggest that roughly 60% of the phenotypic variation in BPH is accounted for by genetic factors. We used logistic regression to model BPH risk as a function of principal components of ancestry, age, and imputed genotype data, with meta-analysis performed using METAL. The top result was on chromosome 22 in SYN3 at rs2710383 (p-value = 4.6 × 10-7; Odds Ratio = 0.69, 95% confidence interval = 0.55-0.83). Other suggestive signals were near genes GLGC, UNCA13, SORCS1 and between BTBD3 and SPTLC3. We also evaluated genetically-predicted gene expression in prostate tissue. The most significant result was with increasing predicted expression of ETV4 (chr17; p-value = 0.0015). Overexpression of this gene has been associated with poor prognosis in prostate cancer. In conclusion, although there were no genome-wide significant variants identified for BPH susceptibility, we present evidence supporting the heritability of this phenotype, have identified suggestive signals, and evaluated the association between BPH and genetically-predicted gene expression in prostate.

2,258 European ancestry cases, 398 African and unknown ancestry cases, 6,599 European ancestry controls, 1,164 African and unknown ancestry controls

Chapter III

Study Statistics

Key metrics and study information

10419
Total Participants
GWAS
Study Type
No
Replicated
African unspecified, NR, European
Ancestry
U.S.
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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