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GWAS Study

Integrative multi-omics analyses to identify the genetic and functional mechanisms underlying ovarian cancer risk regions.

Dareng EO, Coetzee SG, Tyrer JP et al.

38723632 PubMed ID
GWAS Study Type
129118 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

DE
Dareng EO
CS
Coetzee SG
TJ
Tyrer JP
PP
Peng PC
RW
Rosenow W
CS
Chen S
DB
Davis BD
DF
Dezem FS
SJ
Seo JH
NR
Nameki R
RA
Reyes AL
AK
Aben KKH
AH
Anton-Culver H
AN
Antonenkova NN
AG
Aravantinos G
BE
Bandera EV
BF
Beane Freeman LE
BM
Beckmann MW
BA
Beeghly-Fadiel A
BJ
Benitez J
BM
Bernardini MQ
BL
Bjorge L
BA
Black A
BN
Bogdanova NV
BK
Bolton KL
BJ
Brenton JD
BA
Budzilowska A
BR
Butzow R
CH
Cai H
CI
Campbell I
CR
Cannioto R
CJ
Chang-Claude J
CS
Chanock SJ
CK
Chen K
CG
Chenevix-Trench G
CY
Chiew YE
CL
Cook LS
DA
DeFazio A
DJ
Dennis J
DJ
Doherty JA
DT
Dörk T
DB
du Bois A
DM
Dürst M
ED
Eccles DM
EG
Ene G
FP
Fasching PA
FJ
Flanagan JM
FR
Fortner RT
FF
Fostira F
GA
Gentry-Maharaj A
GG
Giles GG
GM
Goodman MT
GJ
Gronwald J
HC
Haiman CA
HN
Håkansson N
HF
Heitz F
HM
Hildebrandt MAT
HE
Høgdall E
HC
Høgdall CK
HR
Huang RY
JA
Jensen A
JM
Jones ME
KD
Kang D
KB
Karlan BY
KA
Karnezis AN
KL
Kelemen LE
KC
Kennedy CJ
KE
Khusnutdinova EK
KL
Kiemeney LA
KS
Kjaer SK
KJ
Kupryjanczyk J
LM
Labrie M
LD
Lambrechts D
LM
Larson MC
LN
Le ND
LJ
Lester J
LL
Li L
LJ
Lubiński J
LM
Lush M
MJ
Marks JR
MK
Matsuo K
MT
May T
MJ
McLaughlin JR
MI
McNeish IA
MU
Menon U
MS
Missmer S
MF
Modugno F
MM
Moffitt M
MA
Monteiro AN
MK
Moysich KB
NS
Narod SA
NT
Nguyen-Dumont T
OK
Odunsi K
OH
Olsson H
ON
Onland-Moret NC
PS
Park SK
PT
Pejovic T
PJ
Permuth JB
PA
Piskorz A
PD
Prokofyeva D
RM
Riggan MJ
RH
Risch HA
RC
Rodríguez-Antona C
RM
Rossing MA
SD
Sandler DP
SV
Setiawan VW
SK
Shan K
SH
Song H
SM
Southey MC
SH
Steed H
SR
Sutphen R
SA
Swerdlow AJ
TS
Teo SH
TK
Terry KL
TP
Thompson PJ
VT
Vestrheim Thomsen LC
TL
Titus L
TB
Trabert B
TR
Travis R
TS
Tworoger SS
VE
Valen E
VN
Van Nieuwenhuysen E
ED
Edwards DV
VR
Vierkant RA
WP
Webb PM
WC
Weinberg CR
WR
Weise RM
WN
Wentzensen N
WE
White E
WS
Winham SJ
WA
Wolk A
WY
Woo YL
WA
Wu AH
YL
Yan L
YD
Yannoukakos D
ZN
Zeinomar N
ZW
Zheng W
ZA
Ziogas A
BA
Berchuck A
GE
Goode EL
HD
Huntsman DG
PC
Pearce CL
RS
Ramus SJ
ST
Sellers TA
FM
Freedman ML
LK
Lawrenson K
SJ
Schildkraut JM
HD
Hazelett D
PJ
Plummer JT
KS
Kar S
JM
Jones MR
PP
Pharoah PDP
GS
Gayther SA
Chapter II

Abstract

Summary of the research findings

To identify credible causal risk variants (CCVs) associated with different histotypes of epithelial ovarian cancer (EOC), we performed genome-wide association analysis for 470,825 genotyped and 10,163,797 imputed SNPs in 25,981 EOC cases and 105,724 controls of European origin. We identified five histotype-specific EOC risk regions (p value <5 × 10-8) and confirmed previously reported associations for 27 risk regions. Conditional analyses identified an additional 11 signals independent of the primary signal at six risk regions (p value <10-5). Fine mapping identified 4,008 CCVs in these regions, of which 1,452 CCVs were located in ovarian cancer-related chromatin marks with significant enrichment in active enhancers, active promoters, and active regions for CCVs from each EOC histotype. Transcriptome-wide association and colocalization analyses across histotypes using tissue-specific and cross-tissue datasets identified 86 candidate susceptibility genes in known EOC risk regions and 32 genes in 23 additional genomic regions that may represent novel EOC risk loci (false discovery rate <0.05). Finally, by integrating genome-wide HiChIP interactome analysis with transcriptome-wide association study (TWAS), variant effect predictor, transcription factor ChIP-seq, and motifbreakR data, we identified candidate gene-CCV interactions at each locus. This included risk loci where TWAS identified one or more candidate susceptibility genes (e.g., HOXD-AS2, HOXD8, and HOXD3 at 2q31) and other loci where no candidate gene was identified (e.g., MYC and PVT1 at 8q24) by TWAS. In summary, this study describes a functional framework and provides a greater understanding of the biological significance of risk alleles and candidate gene targets at EOC susceptibility loci identified by a genome-wide association study.

23,394 European ancestry cases, 105,724 European ancestry controls

Chapter III

Study Statistics

Key metrics and study information

129118
Total Participants
GWAS
Study Type
No
Replicated
European
Ancestry
Russian Federation, Belarus, Spain, Greece, Canada, Netherlands, Sweden, U.S., Belgium, Norway, Finland, Denmark, Poland, U.K., Australia, Germany
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

Important Disclaimer: This review has been performed semi-automatically and is provided for informational purposes only. While we strive for accuracy, this analysis may contain errors, omissions, or misinterpretations of the original research. DNA Genics disclaims all liability for any inaccuracies, errors, or consequences arising from the use of this information. Users should independently verify all information and consult original research publications before making any decisions based on this content. This analysis is not intended as a substitute for professional scientific review or medical advice.

Analysis In Progress

Our analysis of this publication is currently being prepared. Please check back soon for comprehensive insights into the health and genetic findings discussed in this research.