Acquired immunodeficiency syndrome (AIDS)-related lymphomas consistently display a B-cell phenotype and are histogenetically related to germinal center (GC) or post-GC B cells in the overwhelming majority of cases. The pathogenesis of AIDS-related lymphoma is a multistep process involving factors provided by the host, as well as alterations intrinsic to the tumor clone. Host factors involved in AIDS-related lymphomagenesis include reduced immunosurveillance particularly against Epstein-Barr virus (EBV)-infected B cells, human immunodeficiency virus (HIV)-induced alteration of endothelial functions, B-cell stimulation and selection by antigen, HIV-induced deregulation of several cytokine loops, and possibly the host's genetic background. The molecular pathways of viral infection and lesions of cancer related genes associated with AIDS-related lymphoma vary substantially in different clinicopathologic categories of the disease and highlight the marked degree of biological heterogeneity of these lymphomas. Although the reasons for the heterogeneity of AIDS-related lymphoma are not totally clear, it is generally believed that the host's background selects for which specific molecular pathway of AIDS-related lymphoma is activated in a given patient. (C) 2000 by W.B. Saunders Company.
|Number of pages||11|
|Journal||Seminars in Oncology|
|Issue number||4 SUPPL.|
|Publication status||Published - 2000|
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