Open AccessHelicobacter pylori eradication to prevent gastric cancer: Underlying molecular and cellular mechanisms
Author(s) -
S. Tsuji,
Masahiko Tsujii,
Hiroaki Murata,
Tsutomu Nishida,
Masato Komori,
Masakazu Yasumaru,
Shuji Ishii,
Yoshiaki Sasayama,
Seiji Kawano,
Norio Hayashi
Publication year - 2006
Publication title -
world journal of gastroenterology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.427
H-Index - 155
eISSN - 2219-2840
pISSN - 1007-9327
DOI - 10.3748/wjg.v12.i11.1671
Subject(s) - helicobacter pylori , carcinogenesis , cancer , gastric mucosa , biology , chronic gastritis , cancer research , metaplasia , population , gastritis , intestinal metaplasia , immunology , epigenetics , stomach , medicine , gene , genetics , environmental health
Numerous cellular and molecular events have been described in development of gastric cancer. In this article, we overviewed roles of Helicobacter pylori (H pylori) infection on some of the important events in gastric carcinogenesis and discussed whether these cellular and molecular events are reversible after cure of the infection. There are several bacterial components affecting gastric epithelial kinetics and promotion of gastric carcinogenesis. The bacterium also increases risks of genetic instability and mutations due to NO and other reactive oxygen species. Epigenetic silencing of tumor suppressor genes such as RUNX3 may alter the frequency of phenotype change of gastric glands to those with intestinal metaplasia. Host factors such as increased expression of growth factors, cytokines and COX-2 have been also reported in non-cancerous tissue in H pylori-positive subjects. It is noteworthy that most of the above phenomena are reversed after the cure of the infection. However, some of them including overexpression of COX-2 continue to exist and may increase risks for carcinogenesis in metaplastic or dysplastic mucosa even after successful H pylori eradication. Thus, H pylori eradication may not completely abolish the risk for gastric carcinogenesis. Efficiency of the cure of the infection in suppressing gastric cancer depends on the timing and the target population, and warrant further investigation.