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Blood, Vol. 95 No. 4 (February 15), 2000:
pp. 1443-1450
Hodgkin and Reed-Sternberg cells represent an expansion of a
single clone originating from a germinal center B-cell with functional
immunoglobulin gene rearrangements but defective immunoglobulin
transcription
Theresa Marafioti,
Michael Hummel,
Hans-Dieter Foss,
Helmut Laumen,
Petra Korbjuhn,
Ioannis Anagnostopoulos,
Hetty Lammert,
Gudrun Demel,
Jan Theil,
Thomas Wirth, and
Harald Stein
Institute of Pathology and Consultation and Reference Centre for
Lymph Node Pathology and Haematopathology, University Hospital Benjamin
Franklin, Free University, Berlin, Germany; Institute of Medical
Radiology and Cell Research, University of Würzburg, Germany.
Single cell studies aimed at clarifying the nature and clonality of
Hodgkin and Reed-Sternberg (HRS) cells of classical Hodgkin's disease
(HD) have so far produced conflicting results. Using an improved single
cell procedure, the HRS cells of 25 patients with nodular sclerosing HD
lacking B- and T-cell antigens, with and without Epstein-Barr virus
infection, were analyzed for the presence of immunoglobulin (Ig) gene
rearrangements. One patient with HD developed follicular lymphoma 2 years later. Both lymphomas originated from a common precursor
identified as a germinal center B cell. The data show that all but one
of the investigated cases harbored rearranged Ig genes, which were
clonal in all instances and carried a high load of somatic mutations.
The Ig coding capacity was preserved in 18 of the 24 cases (75%) with
rearrangements. However, expression of Ig messenger RNA was not
detectable in the HRS cells with the exception of Ig kappa light chain
expression in some tumor cells of 1 case. The lack of Ig gene
transcription in HRS cells was confirmed by analyzing the HD cell lines
L428 and KM-H2 in transient transfection experiments. An Ig
promoter/enhancer reporter construct showed virtually no activity in
these cells compared to 5 control B-cell lines. We conclude that (1)
classical HD is a B-cell lymphoma in most instances, (2) HRS cells are
clonal without any exception, (3) they are derived from germinal center
B-cells that (4) mostly lack crippling mutations but (5) have
consistently lost their Ig gene transcription ability, due to
functional defects in the Ig gene regulatory elements.
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S. Franke, I. Wlodarska, B. Maes, P. Vandenberghe, J. Delabie, A. Hagemeijer, and C. De Wolf-Peeters
Lymphocyte predominance Hodgkin disease is characterized by recurrent genomic imbalances
Blood,
March 15, 2001;
97(6):
1845 - 1853.
[Abstract]
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D. Re, M. Müschen, T. Ahmadi, C. Wickenhauser, A. Staratschek-Jox, U. Holtick, V. Diehl, and J. Wolf
Oct-2 and Bob-1 Deficiency in Hodgkin and Reed Sternberg Cells
Cancer Res.,
March 1, 2001;
61(5):
2080 - 2084.
[Abstract]
[Full Text]
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R. Kuppers, A. Brauninger, M. Muschen, V. Distler, M.-L. Hansmann, and K. Rajewsky
Evidence that Hodgkin and Reed-Sternberg cells in Hodgkin disease do not represent cell fusions
Blood,
February 1, 2001;
97(3):
818 - 821.
[Abstract]
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H. Stein, T. Marafioti, H.-D. Foss, H. Laumen, M. Hummel, I. Anagnostopoulos, T. Wirth, G. Demel, and B. Falini
Down-regulation of BOB.1/OBF.1 and Oct2 in classical Hodgkin disease but not in lymphocyte predominant Hodgkin disease correlates with immunoglobulin transcription
Blood,
January 15, 2001;
97(2):
496 - 501.
[Abstract]
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B. F. Skinnider, A. J. Elia, R. D. Gascoyne, L. H. Trumper, F. von Bonin, U. Kapp, B. Patterson, B. E. Snow, and T. W. Mak
Interleukin 13 and interleukin 13 receptor are frequently expressed by Hodgkin and Reed-Sternberg cells of Hodgkin lymphoma
Blood,
January 1, 2001;
97(1):
250 - 255.
[Abstract]
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T. Spieker, J. Kurth, R. Kuppers, K. Rajewsky, A. Brauninger, and M.-L. Hansmann
Molecular single-cell analysis of the clonal relationship of small Epstein-Barr virus-infected cells and Epstein-Barr virus-harboring Hodgkin and Reed/Sternberg cells in Hodgkin disease
Blood,
November 1, 2000;
96(9):
3133 - 3138.
[Abstract]
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K J Flavell and P G Murray
Hodgkin's disease and the Epstein-Barr virus
Mol. Pathol.,
October 1, 2000;
53(5):
262 - 269.
[Abstract]
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