Abstract
BackgroundTo evaluate the prevalence of more virulent H. pylori genotypes in relatives of gastric cancer patients and in patients without family histories of gastric cancer.MethodsWe evaluated prospectively the prevalence of the infection by more virulent H. pylori strains in 60 relatives of gastric cancer patients comparing the results with those obtained from 49 patients without family histories of gastric cancer. H. pylori status was determined by the urease test, histology and presence of H. pylori ureA. The cytotoxin associated gene (cagA), the cagA-EPIYA and vacuolating cytotoxin gene (vacA) were typed by PCR and the cagA EPIYA typing was confirmed by sequencing.ResultsThe gastric cancer relatives were significant and independently more frequently colonized by H. pylori strains with higher numbers of CagA-EPIYA-C segments (OR = 4.23, 95%CI = 1.53–11.69) and with the most virulent s1m1 vacA genotype (OR = 2.80, 95%CI = 1.04–7.51). Higher numbers of EPIYA-C segments were associated with increased gastric corpus inflammation, foveolar hyperplasia and atrophy. Infection by s1m1 vacA genotype was associated with increased antral and corpus gastritis.ConclusionsWe demonstrated that relatives of gastric cancer patients are more frequently colonized by the most virulent H. pylori cagA and vacA genotypes, which may contribute to increase the risk of gastric cancer.
Highlights
To evaluate the prevalence of more virulent H. pylori genotypes in relatives of gastric cancer patients and in patients without family histories of gastric cancer
Because the s1m1 genotype of the vacuolating cytotoxin gene (vacA) H. pylori was seen to be more frequently observed in the strains of gastric cancer patients, we evaluated the vacA mosaicism in the strains
We demonstrated that relatives of gastric cancer patients are more frequently colonized by H. pylori strains with the most virulent vacA genotype, s1m1, and by CagA-positive strains possessing a higher number of EPIYA-C segments than the H. pylori strains of the patients without a family history of the disease
Summary
To evaluate the prevalence of more virulent H. pylori genotypes in relatives of gastric cancer patients and in patients without family histories of gastric cancer. It is estimated that individuals infected with H. pylori have more than two-fold increased risk of developing gastric cancer compared with non-infected ones [2] Japanese. Several studies have shown an increased risk of developing gastric cancer in relatives of patients with the disease [2,4]. An increased prevalence of precancerous gastric lesions has been observed in relatives of gastric cancer patients [5]. The most investigated H. pylori virulence determinant, the cag-PAI (cytotoxin associated gene pathogenicity island), encodes a type IV secretion system (T4SS) that is responsible for the entrance of an effector protein, CagA, into host gastric epithelial cells [6,7]. CagA forms a physical complex with SHP-2 phosphatase and triggers abnormal cellular signals, which enhance the risk of damaged cells acquiring precancerous genetic changes [8,9]
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