Cancer Survey, 2: 438-450, 1983.
Gastric cancer represents a major health burden worldwide. Its prognosis is dismal in most countries, except in Japan where massive programs of early detection are in place. In most countries the most promising strategy to control the disease is prevention, facilitated by the existence of a prolonged precancerous process. A successful strategy for prevention depends on the identification and understanding of the different stages of the precancerous cascade. The lesion detected earliest is the inflammation of the gastric mucosa, usually linked to H. pylori infection. H. pylori must be eradicated when detected in the presence of gastritis or precancerous lesions, since virulent strains are linked to progression to adenocarcinoma. The inflammatory changes, although frequent, are not specific and are not associated with increased gastric cancer risk. The next stage in the cascade is the loss of glands (MAG) that eventually may be replaced by epithelium with intestinal phenotype. The incomplete type of intestinal metaplasia is clearly associated with a high cancer risk. It has been considered a low-grade dysplasia by some investigators. The extension of the atrophic or metaplastic changes is also an indicator of cancer risk. It can be evaluated with serum PG levels. The final stage of the process, invasive adenocarcinoma, seems to be linked to molecules that have the capacity to degrade the intercellular matrix, such as uPAR. Biomarkers of advanced stages of the cascade hold the promise of a successful cancer prevention program.