Gastric Cancer

Excerpt

Nearly 20 years have elapsed since the discovery of Helicobacter pylori (168). Due to the progress of research during this period, a causal link between H. pylori and gastric mucosal lesions seems almost certain. Experimental ingestion of H. pylori demonstrated that it caused gastritis in humans, with the inflammation being cured by eradication of the organism (103, 109). Furthermore, H. pylori infection is one of the major causes of recurrent peptic ulcer disease (124, 164). Accordingly, patients with peptic ulcer disease are advised to undergo H. pylori eradication therapy.

Gastric cancer is one of the most common malignancies in the world, although the incidence and mortality rate have been decreasing in recent decades. The association between H. pylori and gastric cancer has attracted great interest worldwide because the International Agency for Research on Cancer (IARC), a subordinate organization of the World Health Organization (WHO), identified H. pylori as a "group 1 (definite carcinogen)" in 1994 (1). That is, the IARC concluded that H. pylori was certainly linked to carcinogenesis on the basis of the results of epidemiologic studies.

The association between H. pylori and gastric cancer may be explained by two possible mechanisms: one is based on a carcinogenesis-promoting effect of H. pylori itself and the other is based on the establishment of a carcinogenic environment due to long-term infection with H. pylori. In the second case, although H. pylori may have no carcinogenesis-promoting effect itself, infection causes inflammation of the gastric mucosa and chronic infection causes mucosal atrophy, resulting in intestinal metaplasia. These latter changes are considered precursors of gastric cancer.

Research concerning the association between gastric cancer and H. pylori has achieved enormous progress over time, leading to the recognition of this relationship by the WHO. One of the greatest concerns is to ascertain whether ultimately H. pylori-induced gastritis may lead to gastric cancer. The onset of gastric cancer can be explained as being caused not only by H. pylori infection, but also by a combination of various factors such as food and the environment. However, the possibility that the occurrence of gastric cancer, like the recurrence of peptic ulcer disease, can be prevented by eradication of H. pylori has also been suggested. Further progress in epidemiologic research is needed to resolve this issue.