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GWAS Study

A genome-wide gene-environment interaction analysis for tobacco smoke and lung cancer susceptibility.

Zhang R, Chu M, Zhao Y et al.

24658283 PubMed ID
GWAS Study Type
8431 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

ZR
Zhang R
CM
Chu M
ZY
Zhao Y
WC
Wu C
GH
Guo H
SY
Shi Y
DJ
Dai J
WY
Wei Y
JG
Jin G
MH
Ma H
DJ
Dong J
YH
Yi H
BJ
Bai J
GJ
Gong J
SC
Sun C
ZM
Zhu M
WT
Wu T
HZ
Hu Z
LD
Lin D
SH
Shen H
CF
Chen F
Chapter II

Abstract

Summary of the research findings

Tobacco smoke is the major environmental risk factor underlying lung carcinogenesis. However, approximately one-tenth smokers develop lung cancer in their lifetime indicating there is significant individual variation in susceptibility to lung cancer. And, the reasons for this are largely unknown. In particular, the genetic variants discovered in genome-wide association studies (GWAS) account for only a small fraction of the phenotypic variations for lung cancer, and gene-environment interactions are thought to explain the missing fraction of disease heritability. The ability to identify smokers at high risk of developing cancer has substantial preventive implications. Thus, we undertook a gene-smoking interaction analysis in a GWAS of lung cancer in Han Chinese population using a two-phase designed case-control study. In the discovery phase, we evaluated all pair-wise (591 370) gene-smoking interactions in 5408 subjects (2331 cases and 3077 controls) using a logistic regression model with covariate adjustment. In the replication phase, promising interactions were validated in an independent population of 3023 subjects (1534 cases and 1489 controls). We identified interactions between two single nucleotide polymorphisms and smoking. The interaction P values are 6.73 × 10(-) (6) and 3.84 × 10(-) (6) for rs1316298 and rs4589502, respectively, in the combined dataset from the two phases. An antagonistic interaction (rs1316298-smoking) and a synergetic interaction (rs4589502-smoking) were observed. The two interactions identified in our study may help explain some of the missing heritability in lung cancer susceptibility and present strong evidence for further study of these gene-smoking interactions, which are benefit to intensive screening and smoking cessation interventions.

1,506 Han Chinese ancestry smoker cases, 825 Han Chinese ancestry non-smoker cases, 1,309 Han Chinese ancestry smoker controls, 1,768 Han Chinese ancestry non-smoker controls

Chapter III

Study Statistics

Key metrics and study information

8431
Total Participants
GWAS
Study Type
Yes
Replicated
912 Han Chinese ancestry smoker cases, 622 Han Chinese ancestry non-smoker cases, 572 Han Chinese ancestry smoker controls, 917 Han Chinese ancestry non-smoker controls
Replication Participants
East Asian
Ancestry
China
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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