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- W2100023080 abstract "Early gastric mucosa-associated lymphoid tissue (MALT) lymphoma is considered as an antigen-dependent disease associated with long standing antigenic stimulation by Helicobacter pylori (H. pylori) which induces chronic immune response and lymphoid tissue development at the gastric mucosa normally devoid of lymphoid tissue. With disease progression, antigen-independent clones occur via genetic alterations inducing aberrant activation of nuclear factor κB (NF-κB) pathway which is essential for regulation of normal lymphocyte development and activation. Four major translocations, including t (11;18)/API2-MALT1, t (1;14)/BCL10-IGH, t (14;18)/(IGH-MALT1 and t (3;14)/FOXP1-IGH, occur mutually exclusively and lead to generation of cIAP2-MALT1 fusion protein or overexpression of BCL10, MALT1 and Foxp1. Translocation t (3;14)(q27;q32)/BCL6-IGH and t (1;2)(p22;p12)/BCL10-IGκL also occur in some MALT lymphomas. Mutational inactivation of A20, global NF-κB inhibitor, involve the development of especially translocation-negative MALT lymphoma. Downstream effects of most genetic alteration converge on the same NF-κB mediated oncogenic pathway. This review discusses the current advances in the pathophysiology underlying the development of gastric MALT lymphoma and its progression. (Korean J Med 2012;83:689-698) Keywords: H. pylori; Mucosa-associated lymphoid tissue; Gastric MALT lymphoma; Pathophysiology" @default.
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- W2100023080 date "2012-01-01" @default.
- W2100023080 modified "2023-10-18" @default.
- W2100023080 title "Pathophysiology of Gastric MALT Lymphoma" @default.
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- W2100023080 doi "https://doi.org/10.3904/kjm.2012.83.6.689" @default.
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