Aims
The Helicobacter pylori (H. pylori) is considered as the major cause of gastric cancer. This can be explained by the differences in the genotype of the CagA toxicity and the genes of the CagPAI assembly.
Methods
A case control study was conducted among Mongolian adult patients. Gastric endoscopy, gastric histology, H. pylori isolation, and its gene sequence were performed in gastric cancer and non-gastric cancer cases. Тhe diagnosis of gastric cancer was determined by the Lawrence classification. After culturing H.pylori infection DNA was extracted. Based on whole genome database the CagPAI complex genes were extracted and statistically processed.
Results
A total of 54 patients were included in the study, with a male-to-female ratio of 1:1. Among the participants, 27.8% (n=15) were diagnosed with gastric cancer and 72.2% (n=39) had non-cancer cases. According to the updated Sydney classification, 66.7% (n=26) of non-cancer cases were low-risk and 33.3% (n=13) were high-risk for gastric cancer. Cancer prevalence differed by sex: 13.3% of women (n=4) and 45.8% of men (n=11) had cancer, indicating a significantly higher risk in men with H. pylori infection (p=0.009).
Analysis of the H. pylori CagPAI gene revealed that 64.8% (n=35) of cases had complete gene sequences, 20.4% (n=11) were incomplete, and 14.8% (n=8) were negative. Full CagPAI expression was observed in 46.2% of low-risk, 61.5% of high-risk non-cancer groups, and 100% of cancer cases, demonstrating a significant association with gastric pathology (p=0.005). Full gene expression correlated with tumor presence and increased Sydney scores, reflecting greater histopathological changes in the gastric antrum (monocyte score p<0.0001, neutrophil score p<0.001).
Full CagPAI gene expression was associated with a 1.75-fold increased risk of gastric cancer (OR=1.75, 95% CI 1.3–2.3). Individuals over 40 years old with H. pylori infection had a 10.8-fold higher risk (OR=10.8, 95% CI 1.3–90.5), and men with H. pylori infection had a 5.5-fold higher risk compared to women (OR=5.5, 95% CI 1.5–20.7).
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Conclusions
1. Among H. pylori–positive patients, 66.7%(n=26) of non-cancer cases were low-risk and 33.3%(n=13) were high-risk according to the updated Sydney classification.
2. Full CagPAI gene expression was observed in 46.2%(n=12)of low-risk, 61.5%(n=8) of high-risk, and 100% of cancer cases, indicating a strong association with gastric cancer development (p=0.005).