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Blood, 1 August 2005, Vol. 106, No. 3, pp. 1031-1036.
Prepublished online as a Blood First Edition Paper on April 19, 2005; DOI 10.1182/blood-2005-01-0168.
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Submitted January 13, 2005
Accepted March 28, 2005
Immunoglobulin gene analysis reveals two distinct cells of origin for EBV positive and EBV negative Burkitt's lymphomas
Cristiana Bellan, Stefano Lazzi, Michael Hummel, Nazzareno Palummo, Margherita de Santi, Teresa Amato, Joshua Nyagol, Elena Sabattini, Thierry Lazure, Stefano A Pileri, Martine Raphael, Harald Stein, Piero Tosi, and Lorenzo Leoncini*
Department of Human Pathology and Oncology, University of Siena, Siena, Italy
Institut fur Pathologie, Charite - Campus Benjamin Franklin, Berlin, Germany
Department of Human Pathology and Oncology, University of Siena, Siena, Italy; Department of Human Pathology, Nairobi Hospital, Nairobi, Kenya
'L.A. Scragnoli' Haematopathology Unit, Policlinico S. Orsola, Bologna, Italy
Hematology, Bicetre Hospital, INSERM E109, University Paris XI, Paris, France
* Corresponding author; email: leoncinil{at}unisi.it.
The normal counterpart of the neoplastic B cells in Burkitt's lymphomas (BL) is still unclear. Based on immunoglobulin gene rearrangement studies, some authors suggest an origin from germinal center cells and others from memory B cells. However, most of these studies rely on cell lines or a small series of cases. To help clarify the cell of origin of BL, a semi-nested PCR was performed to amplify the VDJ rearrangements of the immunoglobulin heavy chain (VH) genes and the resulting amplificates were sequenced for comparison with known germ line VH segments. The results of this approach revealed that all cases (15 endemic, 10 sporadic and 6 AIDS-related BL) harbor mutated VH genes, with different mutation ranges between the three types of BL. The endemic and AIDS-related forms showed a considerably higher mutation rate than the sporadic form (5.1%, 5.4% and 1.5% respectively). The mutations in eBL and AIDS-related BL also showed signs of antigen selection, while no signs of antigen selection were found in sBL. Finally, after subcloning the amplificates, sequence analysis revealed no signs of ongoing mutations in any of the cases analyzed. Since one of the main differences between eBL and AIDS related BL on the one hand and sBL on the other hand is the association with EBV, we compared EBV-positive and EBV-negative BL, independently of their geographical origin and HIV status. The differences in the number of somatic mutations and antigen selection were even more evident when this approach was used. According to our molecular results, it appears that EBV+ and EBV- BL may originate from two distinct subsets of B cells, pointing to a particular role for the germinal-centre reaction in the pathogenesis of these tumors. The different types of C-MYC translocation reported in BL may also be related to the different stages of B-cell maturation.
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