期刊
LEUKEMIA
卷 23, 期 11, 页码 2129-2138出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/leu.2009.161
关键词
anaplastic large cell lymphoma; Hodgkin lymphoma; gene expression profiling; lymphoma pathogenesis
资金
- Deutsche Forschungsgemeinschaft [KU1315/5-2, BR1238/6-2 and 6-3, WI2015/1-1]
- Deutsche Krebshilfe and the Associazione Italiana per la Ricerca sul Cancro (AIRC)
- German Jose Carreras Leukemia Foundation [F 05/01]
Anaplastic large cell lymphoma (ALCL) is a main type of T-cell lymphomas and comprises three distinct entities: systemic anaplastic lymphoma kinase (ALK) positive, systemic ALK(-) and cutaneous ALK(-) ALCL (cALCL). Little is known about their pathogenesis and their cellular origin, and morphological and immunophenotypical overlap exists between ALK(-) ALCL and classical Hodgkin lymphoma (cHL). We conducted gene expression profiling of microdissected lymphoma cells of five ALK(+) and four ALK(-) systemic ALCL, seven cALCL and sixteen cHL, and of eight subsets of normal T and NK cells. The analysis supports a derivation of ALCL from activated T cells, but the lymphoma cells acquired a gene expression pattern hampering an assignment to a CD4(+), CD8(+) or CD30(+) T-cell origin. Indeed, ALCL display a down-modulation of many T-cell characteristic molecules. All ALCL types show significant expression of NF kappa B target genes and upregulation of genes involved in oncogenesis (e. g. EZH2). Surprisingly, few genes are differentially expressed between systemic and cALCL despite their different clinical behaviour, and between ALK(-) ALCL and cHL despite their different cellular origin. ALK(+) ALCL are characterized by expression of genes regulated by pathways constitutively activated by ALK. This study provides multiple novel insights into the molecular biology and pathogenesis of ALCL. Leukemia (2009) 23, 2129-2138; doi: 10.1038/leu.2009.161; published online 6 August 2009
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