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Blood, 1 November 2005, Vol. 106, No. 9, pp. 3183-3190. Prepublished online as a Blood First Edition Paper on July 26, 2005; DOI 10.1182/blood-2005-04-1399. This Article Full Text (PDF) Supplemental Table and Figure All Versions of this Article: 2005-04-1399v1 106/9/3183    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 Bea, S. Articles by John, P. Search for Related Content PubMed PubMed Citation Articles by Bea, S. Articles by John, P. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted April 5, 2005 Accepted June 29, 2005 Diffuse Large B-Cell Lymphoma Subgroups Have Distinct Genetic Profiles that Influence Tumor Biology and Improve Gene Expression-Based Survival Prediction Silvia Bea, Andreas Zettl, George Wright, Itziar Salaverria, Philipp Jehn, Victor Moreno, Christof Burek, German Ott, Xavier Puig, Liming Yang, Armando Lopez-Guillermo, Wing C Chan, Dennis D Weisenburger, James O Armitage, Randy D Gascoyne, Joseph M Connors, Thomas M Grogan, Rita Braziel, Richard I Fisher, Erlend B Smeland, Stein Kvaloy, Jan Delabie, Richard Simon, Wyndham H Wilson, Elaine S Jaffe, Emili Montserrat, Hans-Konrad Muller-Hermelink, Louis M Staudt, Elias Campo*, Andreas Rosenwald, Greiner C Timothy, Holte Harald, and Powell John Department of Pathology, Hospital Clinic, University of Barcelona, Barcelona, Spain Department of Pathology, University of Wurzburg, Wurzburg, Germany Biometric Research, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD, USA Cancer Epidemiology Service, IDIBELL Catalan Institute of Oncology and Laboratori de Estadistica i Epidemiologia, Faculty of Medicine, Autonomous University of Barcelona, Barcelona, Spain Information and Studies Service, Catalan Department of Health, Barcelona, Spain Bioinformatics and Molecular Analysis Section, CBEL, CIT, National Institutes of Health (NIH), Bethesda, MD, USA Department of Hematology, Hospital Clinic, University of Barcelona, Barcelona, Spain Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE, USA Department of Pathology, British Columbia Cancer Center, Vancouver, Canada Southwest Oncology Group, Oregon Health and Science University, Portland, OR, USA; Department of Pathology and Medicine, University of Arizona Cancer Center, Tucson, AZ, USA Southwest Oncology Group, Oregon Health and Science University, Portland, OR, USA; Department of Pathology, Oregon Health and Science University, Portland, OR, USA James P. Wilmot Cancer Center, University of Rochester School of Medicine, Rochester, NY, USA Department of Immunology, The Norwegian Radium Hospital, Oslo, Norway Department of Oncology, The Norwegian Radium Hospital, Oslo, Norway Department of Pathology, The Norwegian Radium Hospital, Oslo, Norway Medicine Branch, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD, USA Pathology Branch, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD, USA Metabolism Branch, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD, USA * Corresponding author; email: ECAMPO{at}clinic.ub.es. Gene expression profiling has identified three major subgroups of diffuse large B-cell lymphoma (DLBCL): germinal center B cell-like (GCB), activated B cell-like (ABC), and primary mediastinal DLBCL (PMBCL). Using comparative genomic hybridization (CGH) we investigated the genetic alterations of 224 untreated DLBCL (87 GCB-DLBCL, 77 ABC-DLBCL, 19 PMBCL, and 41 unclassified-DLBCL) previously characterized by gene expression profiling. The DLBCL subgroups differed significantly in the frequency of particular chromosomal aberrations. ABC-DLBCL had frequent trisomy 3, gains of 3q and 18q21-q22, and losses of 6q21-q22, whereas GCB-DLBCL had frequent gains of 12q12, and PMBCL gains of 9p21-pter and 2p14-p16. Parallel analysis of CGH alterations, locus-specific gene expression profiles and global gene expression signatures revealed that DNA amplifications and gains had a substantial impact on the expression of genes in the involved chromosomal regions, and some genes were overexpressed in a DLBCL subgroup-specific fashion. Unexpectedly, specific chromosomal alterations were associated with significant changes in gene expression signatures that reflect various aspects of lymphoma cell biology as well as the host response to the lymphoma. In addition, gains involving the chromosomal region 3p11-p12 provided prognostic information that was statistically independent of the previously defined gene expression-based survival model, thereby improving its predictive power. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. J. Bende, F. van Maldegem, and C. J.M. van Noesel Chronic inflammatory disease, lymphoid tissue neogenesis and extranodal marginal zone B-cell lymphomas Haematologica, August 1, 2009; 94(8): 1109 - 1123. [Abstract] [Full Text] [PDF] D. de Jong Novel lymphoid neoplasms - the borderland between diffuse large B-cell lymphoma and Burkitt's lymphoma Haematologica, July 1, 2009; 94(7): 894 - 896. [Full Text] [PDF] S. 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