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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. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-01-0168v1 106/3/1031    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Bellan, C. Articles by Leoncini, L. Search for Related Content PubMed PubMed Citation Articles by Bellan, C. Articles by Leoncini, L. Related Collections Immunobiology Neoplasia Oncogenes and Tumor Suppressors Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Immunoglobulin gene analysis reveals 2 distinct cells of origin for EBV-positive and EBV-negative Burkitt 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 From the Department of Human Pathology and Oncology, University of Siena, Italy; Institut für Pathologie, Charité–Campus Benjamin Franklin, Berlin, Germany; Department of Human Pathology, Nairobi Hospital, Kenya; "L.A. Seragnoli" Haematopathology Unit, Policlinico S. Orsola, Bologna, Italy; and Hematology, Bicêtre Hospital, INSERM E109 University Paris XI, France. The normal counterpart of the neoplastic B cells in Burkitt lymphoma (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 on a small series of cases. To help clarify the cell of origin of BL, semi-nested polymerase chain reaction (PCR) was performed to amplify the VDJ rearrangements of the immunoglobulin heavy chain (VH) genes, and the resultant amplificates were sequenced for comparison with known germline VH segments. The results of this approach revealed that all cases (15 endemic BL [eBL], 10 sporadic BL [sBL], and 6 AIDS-related BL) harbor mutated VH genes, with different mutation ranges among the 3 types of BL. The eBL and AIDS-related forms showed considerably higher mutation rates than the sBL form (5.1%, 5.4%, and 1.5%, respectively). The mutations in eBL and AIDS-related BL also showed signs of antigen selection, whereas 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. Given that 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 Epstein-Barr virus (EBV), we compared EBV-positive and EBV-negative BLs independently of their geographic 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-positive and EBV-negative BL may originate from 2 distinct subsets of B cells, pointing to a particular role for the germinal-center 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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Montes-Moreno, G. Roncador, L. Maestre, N. Martinez, L. Sanchez-Verde, F. I. Camacho, J. Cannata, J. L. Martinez-Torrecuadrada, Y. Shen, W. C. Chan, et al. Gcet1 (centerin), a highly restricted marker for a subset of germinal center-derived lymphomas Blood, January 1, 2008; 111(1): 351 - 358. [Abstract] [Full Text] [PDF] G Brady, G J MacArthur, and P J Farrell Epstein Barr virus and Burkitt lymphoma J. Clin. Pathol., December 1, 2007; 60(12): 1397 - 1402. [Abstract] [Full Text] [PDF] G. De Falco, E. Leucci, D. Lenze, P. P. Piccaluga, P. P. Claudio, A. Onnis, G. Cerino, J. Nyagol, W. Mwanda, C. Bellan, et al. Gene-expression analysis identifies novel RBL2/p130 target genes in endemic Burkitt lymphoma cell lines and primary tumors Blood, August 15, 2007; 110(4): 1301 - 1307. [Abstract] [Full Text] [PDF] J. Stebbing, S. Mandalia, C. Palmieri, M. Nelson, B. Gazzard, and M. Bower Burkitt's Lymphoma and Previous AIDS-Defining Illnesses Are Not Prognostic Factors in AIDS-Related Non-Hodgkin's Lymphoma J. Clin. Oncol., November 20, 2005; 23(33): 8538 - 8540. [Full Text] [PDF]

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