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GWAS research with replication samples is valuable to establish robust evidence of a main genetic effect.
The genotypic values used to calculate the main genetic effect parameters are tabulated as table 5.
We performed screening for overall main genetic effect using allelic association tests (Table 1).
Under a dominant model with a baseline risk of 0.0001 and a genetic relative risk of 0.6, 300 case parent trios have a power of 0.62 to detect a main genetic effect at a 0.05 significance level.
In addition, SNP rs7314308 had small P values for both the main genetic effect (PSNP = 5.43 × 10-5) and the gene by occupational exposure effect (Pinteraction = 1.20 × 10-5).
Kraft et al. [ 81] proposed to screen for top genes in the presence of possible gene-environment interactions using a 2-df test for testing for the main genetic effect and G×E interactions jointly.
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In addition to studies of main genetic effects, a large COPD genetics consortium would improve the statistical power to study gene-by-environment interactions.
Likewise, although epistasis association analysis has been utilized in human genetics [33] [37], all of the main genetic effects and gene interaction effects have not been simultaneously included in one genetic model.
In addition to the main genetic effects, we identified a gene-gene interaction between SMS and SAT1 in conferring risk for anxiety disorders.
For most common diseases, the main genetic effects are expected to be small and therefore would require very large studies to capture [7].
The estimation precision of the main genetic effects, especially three dominance effects, is affected by the size of imprinting effect; a large imprinting effect is associated with poorer estimation precision (Table 4).
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