Copyright ©2006 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Jan 7, 2006; 12(1): 10-16
Published online Jan 7, 2006. doi: 10.3748/wjg.v12.i1.10
Causal role of Helicobacter pylori infection and eradication therapy in gastric carcinogenesis
Masanori Ito, Shinji Tanaka, Tomoari Kamada, Ken Haruma, Kazuaki Chayama
Masanori Ito, Kazuaki Chayama, Department of Medicine and Molecular Science, Hiroshima University, Hiroshima, Japan
Shinji Tanaka, Department of Endoscopy, Hiroshima University Hospital, Hiroshima, Japan
Tomoari Kamada, Ken Haruma, Gastroenterology Unit, Depart-ment of Internal Medicine, Kawasaki Medical School, Kurashiki, Japan
Correspondence to: Shinji Tanaka, MD, PhD, Department of Endoscopy, Hiroshima University Hospital, Hiroshima, 734-8551, Japan. colon@hiroshima-u.ac.jp
Telephone: +81-82-257-5538 Fax: +81-82-257-5538
Received: June 9, 2005
Revised: June 22, 2005
Accepted: June 22, 2005
Published online: January 7, 2006

Many epidemiological reports indicate that Helicobacter pylori (H pylori) infection plays an important role in gastric carcinogenesis. Several genetic and epigenetic alterations contribute to the initiation, promotion, and progression of the cancer cells in a multi-step manner. H pylori is known to induce chronic inflammation in the gastric mucosa. Its products, including superoxides, participate in the DNA damage followed by initiation, and the inflammation-derived cytokines and growth factors contribute to the promotion of gastric carcinogenesis. By eradicating H pylori, gastric inflammation can be cured; the therapy diminishes the levels not only of inflammatory cell infiltration, but also atrophy/intestinal metaplasia in part. A randomized controlled trial revealed that the eradication therapy diminished the gastric cancer prevalence in cases without pre-cancerous conditions. In addition, recent epidemiological studies from Japanese groups demonstrated that the development of gastric cancer, especially of the intestinal type, was decreased by successful eradication therapy, although these were designed in a non-randomized manner. However, it should be mentioned that endoscopic detection is the only way to evaluate the degree of gastric carcinogenesis. We have reported that the endoscopic and histological morphologies could be modified by eradication therapy and it might contribute to the prevalence of gastric cancer development. Considering the biological nature of cancer cell proliferation, it is considered that a sufficiently long-term follow-up would be essential to discuss the anticancer effect of eradication therapy.

Keywords: H pylori, Eradication, Gastritis, Gastric neoplasm, Endoscopy