Investigation shows Helicobacter pylori infection affects mucin phenotype expression in early gastric cancer, suggesting implications for patient treatment.
We investigated the effect of Helicobacter pylori (H. pylori) infection on development of early differentiated gastric cancer with regard to mucin phenotypic expression and cancer’s surrounding mucosa. The H. pylori antibody (HP-Ab) positive rate of patients with gastric cancer was significantly higher than that of control. Furthermore, we classified the gastric cancer group according to mucin histochemistry and immunohistochemistry into 3 types, namely gastric type, intestinal type and gastric-intestinal type whose occurrence rates were 34%, 35% and 31%, respectively. The surrounding mucosa of the intestinal phenotype cancer showed severe atrophy and high degree of intestinal metaplasia but its H. pylori density was very low. On the contrary, the surrounding mucosa of the gastric phenotype cancer revealed mild atrophy and mild intestinal metaplasia whereas the H. pylori density was relatively high. However, no statistically significant difference was observed in HP-Ab positive rate between these cancer types. Moreover, we found that the tumor diameter was inversely correlated with the incidence of the gastric phenotype cancer. These results indicate that intestinal phenotype cancer is related to atrophy and intestinal metaplasia of surrounding mucosa caused by H. pylori infection. Furthermore, we conclude that gastric phenotype cancer is associated with the early stage of H. pylori infection but not atrophy nor intestinal metaplasia.
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Eiraku et al. (2007) studied this question.
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