Effects of agents acting on the renin-angiotensin system on the incidence of gastric cancer: A two-sample Mendelian randomization study

Figures

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  Figure 1.. Diagram for Mendelian randomization (MR). MR is based on 3 hypotheses. First of all, SNPs identified as IVs should be strongly associated with exposure; secondly, selected SNPs must be independent of confounders; and finally, IVs are associated with GC (outcome) only via agents acting on the RAS (exposure), rather than through a direct association. GC = gastric cancer, IVs = instrumental variables, RAS = renin-angiotensin system, SNP = single-nucleotide polymorphism.

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  Figure 2.. Forest plot. Mendelian randomization estimates for the relationship between agents acting on the RAS and GC. CI = confidence interval, GC = gastric cancer, IVW = inverse-variance weighted, OR = odds ratio, RAS = renin-angiotensin system.

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  Figure 3.. (A) Scatter plot of the effects of genetic variants on the agents acting on the RAS and GC. The slopes of the solid lines denote the magnitudes of the associations estimated from the MR analyses. (B) A funnel plot of the causal effect of agents acting on the RAS on GC. (C) Fixed-effect IVW analysis of the causal association of agents acting on the RAS with GC. The black dots and bars indicate the causal estimate and 95% CI using each SNP. The red dot and bar indicate the overall estimate and 95% CI meta-analyzed by the fixed-effect IVW method. (D) Leave-one-out analysis plots for agents acting on the RAS on GC. CI = confidence interval, GC = gastric cancer; MR = Mendelian randomization, IVW = inverse-variance weighted, RAS = renin-angiotensin system, SNP = single-nucleotide polymorphism.