Evidence from pathology and epidemiology studies has been provided for a human model of gastric carcinogenesis with the following sequential stages: chronic gastritis; atrophy; intestinal metaplasia; and dysplasia. The initial stages of gastritis and atrophy have been linked to excessive salt intake and infection with Helicobacter pylori. The intermediate stages have been associated with the ingestion of ascorbic acid and nitrate, determinants of intragastric nitrosation. The final stages have been linked with the supply of β-carotene and with excessive salt intake. Nitrosating agents are candidate carcinogens and could originate in the gastric cavity or in the inflammatory infiltrate.
Presented at the 83rd Annual Meeting of the American Association for Cancer Research, May 22, 1992, San Diego, CA. The work on which a substantial portion of this American Cancer Society lecture is based was supported by Grant P01-CA28842 from the National Cancer Institute, NIH, and represents a collaborative effort with other investigators in the United States and Colombia.