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GWAS Study

Expanding the genetic architecture of nicotine dependence and its shared genetics with multiple traits.

Quach BC, Bray MJ, Gaddis NC et al.

33144568 PubMed ID
GWAS Study Type
91791 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

QB
Quach BC
BM
Bray MJ
GN
Gaddis NC
LM
Liu M
PT
Palviainen T
MC
Minica CC
ZS
Zellers S
SR
Sherva R
AF
Aliev F
NM
Nothnagel M
YK
Young KA
MJ
Marks JA
YH
Young H
CM
Carnes MU
GY
Guo Y
WA
Waldrop A
SN
Sey NYA
LM
Landi MT
MD
McNeil DW
DD
Drichel D
FL
Farrer LA
MC
Markunas CA
VJ
Vink JM
HJ
Hottenga JJ
IW
Iacono WG
KH
Kranzler HR
SN
Saccone NL
NM
Neale MC
MP
Madden P
RM
Rietschel M
MM
Marazita ML
MM
McGue M
WH
Won H
WG
Winterer G
GR
Grucza R
DD
Dick DM
GJ
Gelernter J
CN
Caporaso NE
BT
Baker TB
BD
Boomsma DI
KJ
Kaprio J
HJ
Hokanson JE
VS
Vrieze S
BL
Bierut LJ
JE
Johnson EO
HD
Hancock DB
Chapter II

Abstract

Summary of the research findings

Cigarette smoking is the leading cause of preventable morbidity and mortality. Genetic variation contributes to initiation, regular smoking, nicotine dependence, and cessation. We present a Fagerström Test for Nicotine Dependence (FTND)-based genome-wide association study in 58,000 European or African ancestry smokers. We observe five genome-wide significant loci, including previously unreported loci MAGI2/GNAI1 (rs2714700) and TENM2 (rs1862416), and extend loci reported for other smoking traits to nicotine dependence. Using the heaviness of smoking index from UK Biobank (N = 33,791), rs2714700 is consistently associated; rs1862416 is not associated, likely reflecting nicotine dependence features not captured by the heaviness of smoking index. Both variants influence nearby gene expression (rs2714700/MAGI2-AS3 in hippocampus; rs1862416/TENM2 in lung), and expression of genes spanning nicotine dependence-associated variants is enriched in cerebellum. Nicotine dependence (SNP-based heritability = 8.6%) is genetically correlated with 18 other smoking traits (rg = 0.40-1.09) and co-morbidities. Our results highlight nicotine dependence-specific loci, emphasizing the FTND as a composite phenotype that expands genetic knowledge of smoking.

46,213 European ancestry individuals, 11,787 African American individuals

Chapter III

Study Statistics

Key metrics and study information

91791
Total Participants
GWAS
Study Type
Yes
Replicated
31,854 European ancestry individuals, 1,937 individuals
Replication Participants
European, African American or Afro-Caribbean
Ancestry
Finland, Germany, Italy, U.S., Australia
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.