Pathology of Hodgkin's disease.
This review addresses several current questions about Hodgkin's disease (HD): 1) Does HD represent a single disease or multiple diseases? 2) What is the role of cytokines in HD? 3) What is the nature of the Reed-Sternberg cell? 4) How are Epstein-Barr virus (EBV) and oncogenes (bcl-2, c-myc, and p53) involved in the pathogenesis of HD? Nodular lymphocyte predominance HD appears to be a distinct clinicopathologic entity. Cytokines attract inflammatory cells, induce fibrosis, upregulate oncogenes and adhesion molecules, cause systemic symptoms, and mediate immune suppression. Reed-Sternberg cells are derived from B and T lymphocytes in most instances, although an alternative origin from a follicular dendritic reticulum cell has been proposed. EBV is an etiologic agent in some but not all HD cases. EBV gene products confer a growth advantage on Reed-Sternberg cells. The bcl-2 and p53 oncogenes protect Reed-Sternberg cells from apoptosis and are not directly upregulated by EBV.
Kadin
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Beth Israel Hospital, Boston, Massachusetts.
D016207:Cytokines / Q000502:physiology; D015972:Gene Expression Regulation, Neoplastic; D004854:Herpesvirus 4, Human / Q000302:isolation & purification; D006689:Hodgkin Disease / Q000235:genetics / Q000276:immunology / Q000473:pathology* / Q000821:virology; D006801:Humans; D009857:Oncogenes / Q000235:genetics; D016539:Reed-Sternberg Cells / Q000502:physiology
D016207:Cytokines