Abstract
In the mid-1990s, the demonstration that Helicobacter pylori infection is a risk factor for gastric marginal-zone B-cell lymphoma of MALT type (MALT lymphoma) and the finding that eradication of these bacteria can result in histological lymphoma regression in most patients made this tumor a popular model of antigen-driven lymphomagenesis ( 1 ) . The association of H. pylori with gastric MALT lymphoma led to the hypothesis that the microorganism provides an antigenic stimulus that sustains the growth of the lymphoma in the stomach, and today it is generally accepted that administration of antibiotics to eradicate H. pylori should be the sole initial treatment of gastric MALT lymphoma that is confined to the gastric wall. This approach has been validated in more than 20 reported studies ( 2 ) . These advances in the understanding and treatment of gastric MALT lymphoma prompted a search for microorganisms responsible for the growth of MALT lymphomas outside the stomach. Although Borrelia burgdorferi and Campylobacter jejuni have been associated with marginal-zone lymphomas arising in the skin and small intestine, respectively ( 3 , 4 ) , results implicating particular infectious microorganisms in nongastric lymphomas have often been elusive.