ArticleBMC cancer2025
Quantifying the effects of the Correa pathway from Helicobacter pylori infection to gastric cancer: causal inference found in 6.8 million Koreans.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Association ofFrontiers in cellular and infection microbiology · 2026Article
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4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundThe Correa pathway describes the sequential progression of gastric cancer through Helicobacter pylori (H. pylori) infection, chronic gastritis, atrophic gastritis, intestinal metaplasia, adenoma, and gastric cancer. Clarifying the causal relationships along this pathway can provide robust evidence for targeted gastric cancer preventive strategies.
methodsThis study was conducted using data from the Korean National Health Insurance Service, including 6,863,103 individuals who participated in the National Cancer Screening Program for gastric cancer in 2018, with a 2-year follow-up. We used doubly robust targeted maximum likelihood estimation (TMLE) to quantify the total effect of H. pylori eradication on incident gastric cancer and applied causal mediation analysis (CMA) to evaluate indirect pathways through atrophic gastritis/intestinal metaplasia and adenoma. Analyses were adjusted for age, sex, income, smoking, alcohol use, and family history of gastric cancer.
resultsTMLE revealed that H. pylori infection significantly increased gastric cancer risk (relative risk [RR] = 6.40; 95% confidence interval [CI]: 6.05–6.77), as well as the risk of atrophic gastritis/intestinal metaplasia (RR = 1.41; 95% CI: 1.35–1.43) and adenoma (RR = 5.81; 95% CI: 5.68–5.94). atrophic gastritis/intestinal metaplasia substantially elevated the risk of adenoma (RR = 1.72; 95% CI: 1.67–1.77) and gastric cancer (RR = 1.33; 95% CI: 1.28–1.44). CMA showed that 3% of the H. pylori effect on gastric cancer was mediated through atrophic gastritis/intestinal metaplasia (odds ratio [OR] = 1.03, 95% CI: 1.02–1.04), and 36% was mediated via adenoma (OR = 1.97, 95% CI: 1.94–2.01). Among individuals with atrophic gastritis/intestinal metaplasia, adenoma accounted for 44% of the subsequent gastric cancer risk (OR = 1.13, 95% CI: 1.03–1.34).
conclusionsOur findings demonstrate that H. pylori infection is the most important causal determinant of gastric cancer and adenoma, indicating that prevention of H. pylori is central to gastric cancer prevention.
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