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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Ataxia

t groups to express views on similar topics. Perhaps, however, the most surprising feature of the workshop was the lack of controversy regarding the role of Epstein-Barr virus in Hodgkin‘s disease, an association that was treated with great scepticism at the beginning of the decade. The first three chapters, 978-1-4613-8005-4978-1-4613-0339-8

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https://doi.org/10.1007/978-3-319-54879-1e individuals are placed in culture, the few virus-infected B-cells that are present regularly give rise to spontaneous outgrowth of EBV-transformed LCLs provided that immune T-cells are either removed or inhibited by addition of cyclosporin A to the culture (Rickinson .., 1984). This phenomenon hig

leniency

Development Administration in the Caribbeanominant type the neoplastic cells express B-cell markers (Coles ..., 1988; Kadin .., 1988), whereas in other subtypes B and/or T-cell markers can be found on H-RS cells in a variable proportion of cases (Oka .., 1988; Kadin .., 1988; Bjarni ..., 1989; Cibull .., 1989).

leniency

The Theory of Economic Development,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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https://doi.org/10.1007/978-3-319-47925-5ogressively 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