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Prepublished online as a Blood First Edition Paper on August 7, 2003; DOI 10.1182/blood-2003-05-1683. This Article Full Text (PDF) All Versions of this Article: 2003-05-1683v1 102/10/3775    most recent Alert me when this article is cited Alert me if a correction is posted 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 Capello, D. Articles by Gaidano, G. Search for Related Content PubMed PubMed Citation Articles by Capello, D. Articles by Gaidano, G. Social Bookmarking                   What's this? Submitted May 27, 2003 Accepted July 12, 2003 Molecular histogenesis of posttransplant lymphoproliferative disorders Daniela Capello, Michaela Cerri, Giuliana Muti, Eva Berra, Pierluigi Oreste, Clara Deambrogi, Davide Rossi, Giampietro Dotti, Annarita Conconi, Mario Vigano, Umberto Magrini, Giovanbattista Ippoliti, Enrica Morra, Annunziata Gloghini, Alessandro Rambaldi, Marco Paulli, Antonino Carbone, and Gianluca Gaidano* Hematology Unit, Department of Medical Sciences and IRCAD, Amedeo Avogadro University of Eastern Piedmont, Novara, Italy Division of Hematology, Ospedale Niguarda Ca' Granda, Milan, Italy Division of Pathology, Ospedale Niguarda Ca' Granda, Milan, Italy Division of Hematology, Ospedali Riuniti, Bergamo, Italy Cardiac Surgery Unit, IRCCS Policlinico San Matteo, University of Pavia, Pavia, Italy Department of Pathology, IRCCS Policlinico San Matteo, University of Pavia, Pavia, Italy Division of Internal Medicine, Ospedale Civile di Voghera A.O. Pavia, Voghera, Italy Division of Pathology, Centro di Riferimento Oncologico, Aviano, Italy * Corresponding author; email: gaidano{at}med.unipmn.it. Posttransplant lymphoproliferative disorders (PTLD) represent a serious complication of solid organ transplantation. This study assessed the molecular histogenesis of 52 B cell monoclonal PTLD, including 12 polymorphic PTLD (P-PTLD), 36 diffuse large B cell lymphoma (DLBCL), and 4 Burkitt/Burkitt-like lymphoma (BL/BLL). Somatic hypermutation (SHM) of IgV genes documented that most monoclonal B cell PTLD (75% P-PTLD, 91.3% DLBCL, 100% BL/BLL) derive from germinal center (GC)-experienced B cells. BCL6 mutations occurred in 25% P-PTLD, 60.6% DLBCL and 75.0% BL/BLL. A first histogenetic category of PTLD (31.2% DLBCL) express the BCL6+/MUM1-/+/CD138- profile and mimick B cells experiencing the GC reaction, as also suggested by ongoing SHM in a fraction of these cases. A second subset of PTLD (66.7% P-PTLD and 31.2% DLBCL) display the BCL6-/MUM1+/CD138- phenotype and mimick B cells that have concluded the GC reaction. A third histogenetic category of PTLD (25.0% P-PTLD and 31.2% DLBCL) shows the BCL6-/MUM1+/CD138+ profile, consistent with preterminally differentiated post-GC B cells. Crippling mutations of IgVH and/or IgVL genes, leading to sterile rearrangements and normally preventing cell survival, occur in 4 DLBCL and 1 BL/BLL that may have been rescued from apoptosis through expression of EBV-encoded LMP1. Overall, the histogenetic diversity of monoclonal B cell PTLD may help define biologically homogeneous categories of the disease. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Paulli, L. Arcaini, M. Lucioni, E. Boveri, D. Capello, F. Passamonti, M. Merli, S. Rattotti, D. Rossi, R. Riboni, et al. 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