Abstract

Although most gastric cancers are first detected after the fifth decade of life, they represent the end product of a prolonged precancerous process initiated during childhood as a consequence of the infection of the mucosa with Helicobacter pylori. The initial phase of the process consists of active non-atrophic gastritis. The following stages are: multifocal atrophic gastritis, intestinal metaplasia (initially of complete type, then incomplete type), dysplasia and finally invasive carcinoma. The progression of the lesions is modulated by other factors such as the diet: excessive salt intake accelerates the process while fresh fruits and vegetables play a protective role. In addition, the geographic location influences the process. In Colombia, the high altitude Andes mountains dwellers display more advanced lesions than the residents of the Pacific coast. It appears that the ancestral origin of the infecting H. pylori strains have a determining influence on their capacity to induce precancerous lesions. The H. pylori strains infecting the mountain dwellers are of predominantly European phylogeographic origin. The H. pylori strains infecting the Pacific coast dwellers are predominantly of African origin, probably less virulent. Chemoprevention trials have been partially effective, when the precancerous lesions are not too advanced. Such trials may not eliminate the infection but have a tendency to eliminate preferentially the most virulent bacterial strains.

Keywords: Gastric Precancerous Lesions; Gastric Cancer; Gastric Adenocarcinoma; Helicobacter pylori; Gastric Atrophy; Multifocal Atrophic Gastritis; Intestinal Metaplasia; Dysplasia; Surveillance