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Blood, Vol. 92 No. 7 (October 1), 1998:
pp. 2220-2228
Expression Status of BCL-6 and Syndecan-1 Identifies Distinct
Histogenetic Subtypes of Hodgkin's Disease
Antonino Carbone,
Annunziata Gloghini,
Gianluca Gaidano,
Silvia Franceschi,
Daniela Capello,
Hans G. Drexler,
Brunangelo Falini, and
Riccardo Dalla-Favera
From the Division of Pathology, Centro di Riferimento Oncologico,
IRCCS, Istituto Nazionale Tumori, Aviano, Italy; the Division of
Internal Medicine, the Department of Medical Sciences, University of
Torino at Novara, Novara, Italy; the Division of Epidemiology, Centro
di Riferimento Oncologico, IRCCS, Istituto Nazionale Tumori, Aviano,
Italy; the German Collection of Microorganisms & Cell Cultures, Human
and Animal Cell Culture Collection, Braunschweig, Germany; the
Institute of Hematology, University of Perugia, Italy; and the Division
of Oncology, the Department of Pathology, College of Physicians and
Surgeons, Columbia University, New York, NY.
The tumor cells in most cases of Hodgkin's disease (HD) have been
recently recognized to originate from the B-cell lineage, but their
precise differentiation stage is not fully clarified. Recently, we have
reported that the histogenesis of B-cell lymphomas may be assessed by
monitoring the expression pattern of BCL-6, a transcription factor
expressed in germinal center (GC) B cells, and CD138/syndecan-1
(syn-1), a proteoglycan associated with post-GC, terminal B-cell
differentiation. In this study, we have applied these two markers to
the study of HD histogenesis. We have found that in nodular lymphocyte
predominance HD (NLPHD) tumor cells consistently display the
BCL-6+/syn-1 phenotype, indicating their
derivation from GC B cells. Conversely, classic HD (CHD) is
heterogeneous because the tumor cells of a fraction of CHD display the
BCL-6/syn-1+ phenotype of post-GC B-cells,
whereas another fraction of CHD is constituted by a mixture of tumor
cells reflecting the GC (BCL-6+/syn-1) or
post-GC (BCL-6/syn-1+) phenotypes.
BCL-6/syn-1+ tumor cells of CHD are mostly
found surrounded by T cells expressing CD40L, consistent with the
observation that CD40 signaling downregulates BCL-6 expression. These
data indicate that tumor cells of NLPHD uniformly display a GC B-cell
phenotype, whereas the phenotype of tumor cells of CHD appears to be
modulated by the surrounding cellular background, particularly
CD40L+ reactive T cells.
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