The molecular basis of acquired immunodeficiency syndrome-related lymphomagenesis.
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 one. 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.
Gaidano
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Department of Medical Sciences, Amedeo Avogadro University of Eastern Piedmont, Novara, Italy.
Capello
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Carbone
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D001402:B-Lymphocytes / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D004268:DNA-Binding Proteins; D004854:Herpesvirus 4, Human; D006801:Humans; D007108:Immune Tolerance; D016483:Lymphoma, AIDS-Related / Q000209:etiology* / Q000235:genetics / Q000276:immunology / Q000821:virology; D011518:Proto-Oncogene Proteins; D051560:Proto-Oncogene Proteins c-bcl-6; D019713:Receptors, CCR5; D014157:Transcription Factors
D016207:Cytokines; D004268:DNA-Binding Proteins; D011518:Proto-Oncogene Proteins; D051560:Proto-Oncogene Proteins c-bcl-6; D019713:Receptors, CCR5; D014157:Transcription Factors