Abstract
While the aetiology of Hodgkin’s disease remains unknown, the biology of the disease confirms neoplastic behaviour. Cytogenetic studies suggest that the Reed-Sternberg cells, for which this disease was originally named, represent the malignant cells in Hodgkin’s disease. Most authorities believe that this cell is lymphocytic in origin, coming from activated B- or T-lymphocytes. It appears that the Hodgkin’s cell is derived from an immature lymphoid stage of differentiation prior to or during B- or T-cell receptor gene rearrangement [1]. There are many possible sources of transformation in Hodgkin’s cells, including cytogenetic abnormalities, evidence for proto-oncogene involvement and Epstein-Barr virus infection and/or activation. The heterogeneity of the clinical and histological appearance of Hodgkin’s disease and the multitude of different and controversial cellular markers might be explained by the theory that Hodgkin’s disease is a group of aetio-pathophysiologically associated but not identical disease entities.
This research was supported in part by grant CA-34233 from the National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
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Donaldson, S.S., Oberlin, O. (1992). Hodgkin’s Disease. In: Voûte, P.A., Barrett, A., Lemerle, J. (eds) Cancer in Children. UICC International Union Against Cancer. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84722-6_14
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DOI: https://doi.org/10.1007/978-3-642-84722-6_14
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