Intestinal Metaplasia Related to Gastric Cancer: An Outcome Analysis of Biomarkers for Early Detection

Abstract

Although the overall incidence of gastric cancer is decreasing worldwide, it is the main cause of cancer death both worldwide and in East Asia including Japan. Gastric cancer is histologically divided into two types, intestinal and diffuse types (Lauren, 1965). Helicobact‐ er pylori (H. pylori) infection is considered to be a major risk factor for the development of intestinal-type gastric cancer (Correa, 1990; Sipponen & Hyvarinen, 1993; International Agency for Research on Cancer [IARC], 1994; Graham, 2000; Uemura et al., 2001). It has been postulated that H. pylori infection causes chronic gastritis, gastric atrophy, usually with gastric intestinal metaplasia (IM) and dysplasia, and finally gastric cancer. The stepwise course of this inflammatory process, which usually continues over decades, has been de‐ fined as a sequence of histological events that confer an increasing risk of malignant trans‐ formation, as described in Correa’s hypothesis (Correa, 1995). Long-term interactions between H. pylori infection and human increase the risk for precancerous lesions such as atrophic gastritis and IM (Peek & Blaser, 2002; Mera et al., 2005). Based on several long-term prospective studies involving large groups of patients, it is believed that eradication of H. pylori infection may prevent the development of gastric cancer (Uemura et al., 2001; Mera et al., 2005; You et al., 2000; Take et al., 2005). According to a prospective, randomized, place‐ bo-controlled, population-based study from China, H. pylori eradication significantly de‐ creased the development of gastric cancer in participants without precancerous lesions, i.e., gastric atrophy, IM, or gastric dysplasia (Wong et al., 2004). Furthermore, it has been report‐ ed from Japan that H. pylori treatment reduces the risk of developing new gastric carcinoma in patients who have a history of gastric cancer and are thus at high risk for such develop‐