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Biology of Hodgkin s lymphoma Kuppers R; Schwering I; Brauninger A; Rajewsky K; Hansmann MLAnn Oncol 2002[]; 13 Suppl 1 (ä): 11-8Significant progress has been made in recent years in our understanding of the cellular origin of Hodgkin and Reed-Sternberg (HRS) cells in Hodgkin's lymphoma (HL). It is now clear that in most instances HRS cells represent clonal populations of transformed germinal centre (GC) B cells. While the tumour cells in the lymphocyte predominant type of the disease resemble mutating and antigen-selected GC B cells, there is evidence that HRS cells in classical HL originate from pre-apoptotic GC B cells. HRS cells of the recently defined novel subtype lymphocyte-rich classical HL moleculary resemble HRS cells of the other types of classical HL, but there appear to be phenotypic differences. In rare cases, HRS cells derive from T cells. In contrast to previous speculations, cell fusion apparently does not play a role in the generation of the tumour clone. By gene expression profiling of HL cell lines, it became evident that HRS cells have lost most of the B cell-typical gene expression program, which may explain why these cells can persist without B cell receptor expression and which suggests that at least one of the transforming events involved in HL pathogenesis affects a master regulator of cell lineage identity.|Animals[MESH]|B-Lymphocytes/pathology[MESH]|Clone Cells[MESH]|Gene Expression[MESH]|Gene Rearrangement[MESH]|Hodgkin Disease/genetics/*pathology[MESH]|Humans[MESH]|Reed-Sternberg Cells/pathology[MESH]|T-Lymphocytes/pathology[MESH] |
