Proliferating cell nuclear antigen (PCNA) expression in Hodgkin's disease

Previous studies of the proliferating cell fraction in Hodgkin's disease (HD) have been directed towards the classical Hodgkin and Reed–Sternberg cells (HRS) to the exclusion of the background population and have not included cases of nodular lymphocyte predominant Hodgkin's disease (NLPHD...

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Veröffentlicht in:The Journal of pathology 1992-09, Vol.168 (1), p.1-6
Hauptverfasser: Schmid, Christine, Sweeney, Edel, Isaacson, Peter G.
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Sprache:eng
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Zusammenfassung:Previous studies of the proliferating cell fraction in Hodgkin's disease (HD) have been directed towards the classical Hodgkin and Reed–Sternberg cells (HRS) to the exclusion of the background population and have not included cases of nodular lymphocyte predominant Hodgkin's disease (NLPHD). Using an antibody to proliferating cell nuclear antigen (PCNA), we have determined the growth fraction of HRS cells and L&H cells in paraffin sections of 15 cases of classical HD [12 nodular sclerosis (NS), 3 mixed cellularity (MC)] and eight cases of NLPHD. By double staining with anti‐PCNA and antibodies to B cells (CD20) and T cells (CD45RO), we also determined the growth fraction and immunophenotype of the background population in each case. In classical HD, 50·4 per cent of HRS cells were PCNA‐positive and judged to be proliferating, which is comparable to previous studies, while in NLPHD 76·9 per cent of L&H cells were PCNA‐positive. In both classical HD and NLPHD, the majority of PCNA‐positive cells in the background were T cells, which showed a growth fraction of 57·8 and 68·5 per cent, respectively; in comparison, only 4 per cent of B cells were PCNA‐positive in each type of HD. L&H cells are widely accepted to be B cells and there is growing evidence that HRS cells are also B cell‐derived. Our results underline a relationship between classical HD and NLPHD and suggest that the characteristic histological features of both diseases may be caused by the production and release of cytokines from altered B cells.
ISSN:0022-3417
1096-9896
DOI:10.1002/path.1711680102