Annals of Oncology 13:11-18, 2002
© 2002 European Society for Medical Oncology
Biology of Hodgkin's lymphoma
1 Institute for Genetics 2 Department of Internal Medicine I, University of Cologne, Cologne 3 Department of Pathology, University of Frankfurt, Frankfurt/Main, Germany
Abstract
Significant 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.
angioimmunoblastic lymphadenopathy; cell fusion; composite lymphoma; Hodgkin's lymphoma; Reed–Sternberg cell; somatic hypermutation
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