DESCRIPTION:

List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Esophageal cancer (alcohol interaction). The EFO term esophageal carcinoma was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.

LABEL:

GWAS: esophageal carcinoma

SCORE TYPE:

P-Value

DATE ADDED:

2017-05-02

DATE UPDATED:

2024-04-25

SPECIES:

AUTHORS:

C Wu, P Kraft, K Zhai, J Chang, Z Wang, Y Li, Z Hu, Z He, W Jia, CC Abnet, L Liang, N Hu, X Miao, Y Zhou, Z Liu, Q Zhan, Y Liu, Y Qiao, Y Zhou, G Jin, C Guo, C Lu, H Yang, J Fu, D Yu, ND Freedman, T Ding, W Tan, AM Goldstein, T Wu, H Shen, Y Ke, Y Zeng, SJ Chanock, PR Taylor, D Lin

TITLE:

Genome-wide association analyses of esophageal squamous cell carcinoma in Chinese identify multiple susceptibility loci and gene-environment interactions.

JOURNAL:

Nature genetics Oct 2012, Vol 44, pp. 1090-7

ABSTRACT:

We conducted a genome-wide association study (GWAS) and a genome-wide gene-environment interaction analysis of esophageal squamous-cell carcinoma (ESCC) in 2,031 affected individuals (cases) and 2,044 controls with independent validation in 8,092 cases and 8,620 controls. We identified nine new ESCC susceptibility loci, of which seven, at chromosomes 4q23, 16q12.1, 17q21, 22q12, 3q27, 17p13 and 18p11, had a significant marginal effect (P=1.78×10(-39) to P=2.49×10(-11)) and two of which, at 2q22 and 13q33, had a significant association only in the gene-alcohol drinking interaction (gene-environment interaction P (PG×E)=4.39×10(-11) and PG×E=4.80×10(-8), respectively). Variants at the 4q23 locus, which includes the ADH cluster, each had a significant interaction with alcohol drinking in their association with ESCC risk (PG×E=2.54×10(-7) to PG×E=3.23×10(-2)). We confirmed the known association of the ALDH2 locus on 12q24 to ESCC, and a joint analysis showed that drinkers with both of the ADH1B and ALDH2 risk alleles had a fourfold increased risk for ESCC compared to drinkers without these risk alleles. Our results underscore the direct genetic contribution to ESCC risk, as well as the genetic contribution to ESCC through interaction with alcohol consumption. PUBMED: 22960999
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