Titlebook: Etiology of Hodgkin’s Disease; Ruth F. Jarrett Book 1995 Springer Science+Business Media New York 1995 Antigen.Pathogene.epidemiological.e

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Nripendra Kishore Mishra,Manish Kumar Singhattern of EBV gene expression to the HD-derived tumours. Three centroblastic and one immunoblastic lymphoma derived tumours were EBV-negative. These showed a near identical B-cell phenotype to original biopsies and showed identical immunoglobulin gene rearrangements to the original tumours. Tumours

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,Evidence of an Increased Frequency of HLA-DPB1*0301 in Hodgkin’s Disease Supports an Infectious Aetrease in *0401, and possibly *0501, in HDMC and HDLP. Analysis of *0301-like hypervariable region (HVR) associations with HD subtypes indicated an increase in an *0301-like HVR-C motif in HDNS, but not in non-HDNS. The frequency of *0301- and *0401 -like HVR-C and HVR-F amino acid residues also diff

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,What Can we Learn About the Aetiology of Hodgkin’s Disease from Family Studies?,posure, the number of new melanomas and dysplastic nevi decrease in the individuals following skin care guidelines (Tucker, 1986). In nasopharyngeal carcinoma, the genetic aspects and the environmental aspects remain speculative. HLA loci have been linked to a putative disease-susceptibility gene in

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,Hodgkin’s Disease and Human Herpesvirus-6: A Model for Studies of New Aetiological Agents,ar .., 1991; Levine .., 1992a) and virological (Torelli .., 1991; Gompels .., 1993) studies. This report will summarise the data suggesting an aetiological association, review relevant studies to place these findings in perspective, and discuss possible approaches to the identification of other cand

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Propagation of Hodgkin and Reed-Sternberg Cells,ogressively from 3 of 15 HD biopsy specimens transplanted into SCID mice. The tumours were derived from EBV-positive bystander cells. In 5/6 tumours examined cytogenetically, chromosomal aberrations were detected. We conclude that these bystander cells might differ from normal lymphocytes and possib

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