| pubmed-article:8705260 | pubmed:abstractText | Recent studies indicate that chronic gastritis induced by Helicobacter pylori infection is a predisposing condition for the development of both gastric adenocarcinoma and primary gastric B-cell mucosal associated lymphoid tissue (MALT) lymphoma. The chronic gastritis induced by H pylori may evolved in specific individuals in response to additional genetic, environmental, and bacterial-virulence factors. The transitions from chronic gastritis to gastric atrophy with small intestinal (type I) metaplasia, incomplete small intestinal (type II) metaplasia, large intestinal (type III) metaplasia, low-grade dysplasia, and finally high-grade dysplasia are associated with respectively increasing cancer risk. H pylori infection may also lead to the development of an abnormal clone of B-cells and formation of low-grade MALT lymphoma, which is thought to be a precursor for the development of metastatic high-grade MALT lymphoma. In some patients, low grade MALT lymphoma has been shown to regress after eradication of the H pylori infection. The specific genetic abnormalities associated with these premalignant stages of gastric carcinogenesis are currently being defined. Other conditions associated with an increased risk of gastric adenocarcinoma include autoimmune atrophic gastritis, adenomatous polyps, postgastrectomy remnants, and possibly Ménétrier's disease. | lld:pubmed |
