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Abstract
The development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma depends critically on Helicobacter pylori infection. The bacterial infection stimulates the lymphoma B-cells through both direct (auto-antigen) and indirect (H. pylori specific intra-tumour T-cells) immunological stimulation. It also promotes the acquisition of genetic abnormality through activated neutrophils, which release oxygen reactive species. Malignant clones bearing t(11;18)(q21;q21) form lymphomas that are H. pylori growth independent. Those without t(11;18)(q21;q21) but with other genetic abnormality such as trisomy 3 depend critically on H. pylori mediated immune response at early stages and are therefore responsive to H. pylori eradication. However, at late stages when additional genetic defects such as t(1;14)(p22;q32) accumulate, the tumour may escape its growth dependence on H. pylori mediated immune response. Detection of these chromosomal translocations has significant implication in clinical management of patients with gastric MALT lymphoma.