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GWAS Study

A large-scale association study detects novel rare variants, risk genes, functional elements, and polygenic architecture of prostate cancer susceptibility.

Emami NC, Cavazos TB, Rashkin SR et al.

33293427 PubMed ID
GWAS Study Type
208253 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

EN
Emami NC
CT
Cavazos TB
RS
Rashkin SR
CC
Cario CL
GR
Graff RE
TC
Tai CG
MJ
Mefford JA
KL
Kachuri L
WE
Wan E
WS
Wong S
AD
Aaronson D
PJ
Presti J
HL
Habel LA
SJ
Shan J
RD
Ranatunga DK
CC
Chao CR
GN
Ghai NR
JE
Jorgenson E
SL
Sakoda LC
KM
Kvale MN
KP
Kwok PY
SC
Schaefer C
RN
Risch N
HT
Hoffmann TJ
VD
Van Den Eeden SK
WJ
Witte JS
Chapter II

Abstract

Summary of the research findings

To identify rare variants associated with prostate cancer susceptibility and better characterize the mechanisms and cumulative disease risk associated with common risk variants, we conducted an integrated study of prostate cancer genetic etiology in two cohorts using custom genotyping microarrays, large imputation reference panels, and functional annotation approaches. Specifically, 11,984 men (6,196 prostate cancer cases and 5,788 controls) of European ancestry from Northern California Kaiser Permanente were genotyped and meta-analyzed with 196,269 men of European ancestry (7,917 prostate cancer cases and 188,352 controls) from the UK Biobank. Three novel loci, including two rare variants (European ancestry minor allele frequency < 0.01, at 3p21.31 and 8p12), were significant genome wide in a meta-analysis. Gene-based rare variant tests implicated a known prostate cancer gene (HOXB13), as well as a novel candidate gene (ILDR1), which encodes a receptor highly expressed in prostate tissue and is related to the B7/CD28 family of T-cell immune checkpoint markers. Haplotypic patterns of long-range linkage disequilibrium were observed for rare genetic variants at HOXB13 and other loci, reflecting their evolutionary history. In addition, a polygenic risk score (PRS) of 188 prostate cancer variants was strongly associated with risk (90th vs. 40th-60th percentile OR = 2.62, P = 2.55 × 10-191). Many of the 188 variants exhibited functional signatures of gene expression regulation or transcription factor binding, including a 6-fold difference in log-probability of androgen receptor binding at the variant rs2680708 (17q22). Rare variant and PRS associations, with concomitant functional interpretation of risk mechanisms, can help clarify the full genetic architecture of prostate cancer and other complex traits. SIGNIFICANCE: This study maps the biological relationships between diverse risk factors for prostate cancer, integrating different functional datasets to interpret and model genome-wide data from over 200,000 men with and without prostate cancer.See related commentary by Lachance, p. 1637.

14,113 European ancestry cases, 194,140 European ancestry controls

Chapter III

Study Statistics

Key metrics and study information

208253
Total Participants
GWAS
Study Type
No
Replicated
European
Ancestry
U.K.
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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