Cohort formation.

<p>Cohort formation.</p

Baseline characteristics of study participants (before after propensity score 1∶1 matching).

<p>BMI: body mass index;</p><p>CVD: cardiovascular disease;</p><p>PUD: peptic ulcer disease;</p><p>eGFR: estimated glomerular filtration rate;</p><p>HDL: high-density lipoprotein;</p><p>RAAS: renin-angiotensin-aldosterone system;</p><p>CCB: calcium channel blocker.</p><p><i>Note:</i> Conversion factors for units were as follows: hemoglobin in g/dl to g/l, ×10; white blood cell in ×10³/µl to ×10⁹/l, equal; platelets in ×10³/µl to ×10⁹/l, equal; albumin in mg/dl to g/l,×10; cholesterol in mg/dl to mmol/l,×0.02586; triglycerides in mg/dl to mmol/l,×0.01129; HDL-cholesterol in mg/dl to mmol/l,×0.02586; calcium in mg/dl to mmol/l, ×0.2495; phosphorus in mg/dl to mmol/l, ×0.3229; uric acid in mg/dl to µmol/l, ×59.48.</p

Innate Immunity and Non-Hodgkin’s Lymphoma (NHL) Related Genes in a Nested Case-Control Study for Gastric Cancer Risk

<div><h3>Objective</h3><p>Genetic variants regulating the host immune system may contribute to the susceptibility for the development of gastric cancer. Little is known about the role of the innate immunity- and non-Hodgkin’s lymphoma (NHL)-related genes for gastric cancer risk. This nested case-control study was conducted to identify candidate genes for gastric cancer risk for future studies.</p> <h3>Methods</h3><p>In the Discovery phase, 3,072 SNPs in 203 innate immunity- and 264 NHL-related genes using the Illumine GoldenGateTM OPA Panel were analyzed in 42 matched case-control sets selected from the Korean Multi-center Cancer Cohort (KMCC). Six significant SNPs in four innate immunity (<em>DEFA6, DEFB1, JAK3,</em> and <em>ACAA1</em>) and 11 SNPs in nine NHL-related genes (<em>INSL3, CHMP7, BCL2L11, TNFRSF8, RAD50, CASP7, CHUK, CD79B,</em> and <em>CLDN9</em>) with a permutated <em>p</em>-value <0.01 were re-genotyped in the Replication phase among 386 cases and 348 controls. Odds ratios (ORs) for gastric cancer risk were estimated adjusting for age, smoking status, and <em>H. pylori</em> and CagA sero-positivity. Summarized ORs in the total study population (428 cases and 390 controls) are presented using pooled- and meta-analyses.</p> <h3>Results</h3><p>Four SNPs had no heterogeneity across the phases: in the meta-analysis, <em>DEFA6</em> rs13275170 and <em>DEFB1</em> rs2738169 had both a 1.3-fold increased odds ratio (OR) for gastric cancer (95% CIs = 1.1–1.6; and 1.1–1.5, respectively). <em>INSL3</em> rs10421916 and rs11088680 had both a 0.8-fold decreased OR for gastric cancer (95% CIs = 0.7–0.97; and 0.7–0.9, respectively).</p> <h3>Conclusions</h3><p>Our findings suggest that certain variants in the innate immunity and NHL-related genes affect the gastric cancer risk, perhaps by modulating infection-inflammation-immunity mechanisms that remain to be defined.</p> </div

The event-free survival of patients with atherosclerotic cardiovascular disease according to treatment group (A) before and (B) after PS matching.

<p>Atherosclerotic cardiovascular disease occurred more frequently in aspirin users versus non-users.</p

Multivariate Cox proportional analyses for atherosclerotic cardiovascular disease.

<p>Abbreviations: HR: hazards ratio;</p><p>eGFR: estimated glomerular filtration rate;</p><p>CVD: cardiovascular disease;</p><p>RAAS: renin-angiotensin-aldosterone system;</p><p>CCB: calcium channel blocker.</p

The results of the pooled- and meta-analyses including the discovery and replication phases: Association of most significant SNPs in the innate immunity and NHL-related gene variants and gastric cancer risk.

a<p>Cochran’s <i>p</i>-value of heterogeneity between the ORs (95% CIs) of discovery and those of the replication phase.</p>b<p>All ORs were adjusted for age, smoking status (never <i>vs.</i> ever), <i>H. pylori</i> infection (positive <i>vs.</i> negative) and CagA seropositivity (positive <i>vs.</i> negative).</p

Association of aspirin use and cardiovascular disease in subgroups of the matched cohort.

<p>Association of aspirin use and cardiovascular disease in subgroups of the matched cohort.</p

The event-free survival for (A) composite bleeding, (B) all-cause death, (C) a doubling of baseline serum creatinine, and (D) renal death according to treatment group in the matched cohort.

<p>There were no significant differences in the incidence of composite bleeding and the cumulative overall survival rate between aspirin users and non-users. Aspirin users showed a higher incidence of doubling of baseline serum creatinine and an increased renal death rate compared with non-users.</p

The results in the Discovery phase: Innate immunity and NHL-related gene variants and risk of gastric cancer in the Illumina OPA.

a<p>Minor allele frequency among controls.</p>b<p>Chromosome number.</p>c<p>Adjusted FDR-BH <i>p</i>-values calculated by the most significant SNPs of all genes in analysis; <i>p</i> value of cut-off level ≤0.2.</p>d<p>Adjusted for age, smoking status (never vs. ever), history of <i>Helicobacter Pylori</i> infection and CagA seropositivity.</p

General characteristics of gastric cancer cases and controls selected for the screening of 203 innate immunity- and 264 NHL-related candidate genes in the discovery, replication and pooled analyses.

*<p>Statistically significant or **marginally significant in the distribution of cases and controls.</p>a<p>Defined according to the ICD-10 code: Cardia C16.0; Non-cardia C16.1–C16.6; Overlapping C16.8; and Unspecified C16.9.</p