Abstract

This research aimed to determine the association of the combination of H. pylori infection and TP53 codon 72 polymorphism with non-cardia gastric cancer (GC) in Vietnam. A total of 164 patients with non-cardia GC and 164 patients with peptic ulcer disease or functional dyspepsia in controls matched by sex and age were enrolled. H. pylori infection was diagnosed by rapid urease test and polymerase chain reaction (PCR). The cagA gene-positivity and vacA sm subtypes were determined by multiplex PCR. Genotypes of TP53 codon 72 polymorphism were determined by PCR-restriction fragment length polymorphism. The prevalence of H. pylori infection in GC and control group were 61.6% and 55.4%, respectively. The rates of cagA-positive strains in the two H. pylori-positive groups were 80.2% and 71.4%, respectively. There was no statistically significant difference in TP53 codon 72 genotype distribution between GC group (frequencies of Arg/Arg, Arg/Pro and Pro/Pro genotypes were 31.1%, 43.3% and 25.6%, respectively) and controls (29.3%, 52.4% and 18.3%, respectively), p = 0.172. The significant difference in genotype distribution was observed in recessive model (Pro/Pro vs Arg/Arg + Arg/Pro) when stratifying by H. pylori infection (OR = 2.02, 95% CI 1.03-3.96, p = 0.041) and by cagA-positivity (OR = 2.33, 95% CI 1.07-5.07, p = 0.032). This study suggests a synergistic interaction between H. pylori infection, especially cagA-positive H. pylori, and Pro/Pro genotype of TP53 codon 72 polymorphism might play a significant role in the pathogenesis of GC in the Vietnamese population.

Highlights

  • This research aimed to determine the association of the combination of H. pylori infection and TP53 codon 72 polymorphism with non-cardia gastric cancer in Vietnam

  • Intestinal-type and diffusetype gastric cancer (GC) accounted for 56.1% and 37.8%, respectively while 6.1% of patients with GC were typed as indeterminate according to Lauren classification

  • Our data suggest that H. pylori infection, cytotoxin associated gene A (cagA)-positivity, and vacuolating cytotoxin gene A (vacA) genotypes are not helpful as biomarkers to assess the development of GC in Vietnam, in accordance with other studies reporting the difficulty to explain the pathogenesis of GC by H. pylori infection and cagApositivity due to high prevalence of these factors in Asian population [19,30]

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Summary

Introduction

This research aimed to determine the association of the combination of H. pylori infection and TP53 codon 72 polymorphism with non-cardia gastric cancer (GC) in Vietnam. There was no statistically significant difference in TP53 codon 72 genotype distribution between GC group (frequencies of Arg/Arg, Arg/Pro and Pro/Pro genotypes were 31.1%, 43.3% and 25.6%, respectively) and controls (29.3%, 52.4% and 18.3%, respectively), p = 0.172. The significant difference in genotype distribution was observed in recessive model (Pro/Pro vs Arg/Arg + Arg/Pro) when stratifying by H. pylori infection (OR = 2.02, 95% CI 1.03–3.96, p = 0.041) and by cagA-positivity (OR = 2.33, 95% CI 1.07–5.07, p = 0.032). Conclusions: This study suggests a synergistic interaction between H. pylori infection, especially cagA-positive H. pylori, and Pro/Pro genotype of TP53 codon 72 polymorphism might play a significant role in the pathogenesis of GC in the Vietnamese population. The cytotoxin associated gene A (cagA), the vacuolating cytotoxin gene A (vacA) and several other virulent genes of H. pylori have been demonstrated as etiologic factors in gastroduodenal diseases including GC [5].

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