위 MALT 림프종의 병태생리
분야
의약학 > 내과학
저자
강창석 ( Chang Suk Kang ) , 박경신 ( Gyeong Sin Park )
발행기관
대한내과학회
간행물정보
Korean Journal of Medicine(구 대한내과학회지) 2012년, 제83권 제6호, 689~698페이지(총10페이지)
파일형식
42847580.pdf [무료 PDF 뷰어 다운로드]
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    영문초록
    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)
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