title: Molecular biology of gastric MALT lymphoma: application in clinical management.
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.
authors.affiliation: Department of Histopathology, Royal Free and University College Medical School, University of College London, London, UK. m.du@ucl.ac.uk
authors.forename: Ming-Qing
authors.initials: MQ
authors.lastname: Du
mesh_terms: D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000276:immunology; D002869:Chromosome Aberrations; D019468:Disease Management; D016481:Helicobacter Infections / Q000235:genetics / Q000276:immunology / Q000628:therapy; D006801:Humans; D018442:Lymphoma, B-Cell, Marginal Zone / Q000175:diagnosis / Q000209:etiology* / Q000628:therapy; D011379:Prognosis; D013274:Stomach Neoplasms / Q000175:diagnosis / Q000209:etiology* / Q000628:therapy