Effect of Eradication of Helicobacter pylori on the Histology and Cellular Phenotype of Gastric Intestinal Metaplasia

Effects of Helicobacter pylori infection on genetic instability, the aberrant CpG island methylation status and the cellular phenotype in Barrett's esophagus in a Japanese population

“…The underlying mechanism of the reversal of those molecular events after H. pylori treatment remains elusive. According to the findings of previous reports, it is well known that GIN, a promoter methylation and Das-1 reactivity is associated with chronic inflammatory conditions in gastrointestinal diseases such as BE, 44 chronic gastritis 29,31 and inflammatory bowel disease. 45 The decrease in inflammation in the stomach after the cure of the bacteria may be related to these changes, but it may be difficult to clarify those mechanisms in the current study.…”

“…[22][23][24] We, therefore, hypothesized that if H. pylori infection is an important cause of genetic or epigenetic events in BE, then H. pylori eradication may reverse those molecular alterations, thereby halting BE carcinogenesis as well as gastric carcinogenesis. In this study, we evaluated the chronology of genetic, epigenetic events and cellular phenotype, as identified by a monoclonal antibody (mAb) Das-1 (formerly known as 7E 12 H 12 , IgM isotype), which specifically reacts with BE and EAC 25,26 and is strongly associated with small intestinal adenocarcinoma and gastric carcinoma, [27][28][29] in SIM during BE pathogenesis in Japanese individuals with a high rate of H. pylori infection. The effects of the eradication of H. pylori on those molecular alterations and cellular phenotype in SIM were also assessed in a prospective study.…”

The Pathogenesis of Gastric Carcinoma

“…Correa et al have proposed that there is a progression from normal gastric mucosa to carcinoma in high risk populations (29). The initial change is early onset superficial gastritis which, although reversible, is triggered by a variety of agents.…”

Effects of Helicobacter pylori Infection on the Histology, Cellular Phenotype, K-ras Mutations, and Cell Kinetics in Gastric Intestinal Metaplasia in Patients with Chronic Gastritis and Gastric Cancer

“…Indeed, we recently found that cell kinetics and genetic alterations, i.e. microsatellite instability and K-ras mutations in GIM, play a role in the early events leading to gastric carcinogenesis, and H. pylori eradication settled these genetic events during only the onewww.intechopen.com year post-treatment period (Tanaka et al 2006;Watari et al 2008). Thus, we believe that the follow-up period, up to 4 yrs in this study, is enough to investigate the changes in cellular phenotype and neoplastic biomarkers related to carcinogenesis after H. pylori eradication.…”

“…The annual incidence rate of gastric cancer per 100,000 population in various Asian countries, as reported by Parkin et al (Parkin et al, 1997), is very high in the northern parts of Asia, especially in Japan. In this paragraph, we illustrated around our previous studies (Watari et al, 2007;Watari et al, 2008) in the Japanese population, (i) if the eradication of H. pylori affects subsequent (over the course of up to 4 years) histological grade of GIM, (ii) if mAb Das-1 reactivity that identifies colonic phenotype of GIM associated with gastric carcinogenesis changes after eradication of H. pylori, and (iii) to assess the expression of the novel tropomyosin isoform TC22 in GIM before and after H. pylori treatment. p53 expression was also examined, in parallel.…”