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This Article Full Text Full Text (PDF) 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 Joos, S. Articles by Barth, T. F. E. Search for Related Content PubMed PubMed Citation Articles by Joos, S. Articles by Barth, T. F. E. Related Collections Neoplasia Oncogenes and Tumor Suppressors Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 February 2002, Vol. 99, No. 4, pp. 1381-1387 NEOPLASIA Classical Hodgkin lymphoma is characterized by recurrent copy number gains of the short arm of chromosome 2 Stefan Joos, Christiane K. Menz, Gunnar Wrobel, Reiner Siebert, Stefan Gesk, Sibylle Ohl, Gunhild Mechtersheimer, Lorenz Trümper, Peter Möller, Peter Lichter, and Thomas F. E. Barth From Deutsches Krebsforschungszentrum, Abteilung Organisation komplexer Genome, Heidelberg, Germany; Abteilung für Pathologie des Universitätsklinikums Ulm, Germany; Institut für Humangenetik, Universitätsklinikum Kiel, Germany; Pathologisches Institut der Universität Heidelberg, Germany; and Abteilung Innere Medizin, Klinikum der Georg-August-Universität, Göttingen, Germany. Hodgkin- and Reed-Sternberg (HRS) cells microdissected from 41 classical Hodgkin lymphomas (cHL) of 40 patients comprising 8 lymphocyte-rich (cHL-LR), 16 nodular sclerosis (cHL-NS), 15 mixed-cellularity (cHL-MC), and 2 lymphocyte-depletion (cHL-LD) subtypes were analyzed by comparative genomic hybridization for recurrently imbalanced chromosomal subregions. Chromosomal gains most frequently involved chromosome 2p (54%), 12q (37%), 17p (27%), 9p and 16p (24% each), and 17q and 20q (20% each), whereas losses primarily affected chromosome 13q (22%). Using fluorescence in situ hybridization, amplification of the REL oncogene was demonstrated within a distinct 2p15-p16 amplicon. The high frequency of 2p overrepresentations including REL, particularly in cHL-NS (88%), suggests that an alternative mechanism of constitutive activation of nuclear factor NF-B is a hallmark of HRS cells. Hierarchical cluster analysis of chromosomal imbalances revealed a closer relationship among cHL-NS than other subtypes. Furthermore, there is a tendency for different subtypes of cHL-MC tumors characterized by different ages at the time of tumor onset and gain of chromosome 17p. The imbalance pattern of cHL subtypes suggests that different molecular pathways are activated, with REL or other genes on chromosomal band 2p15-p16 playing a fundamental role in the pathogenesis of classical Hodgkin lymphoma. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. T. Bolisetty, G. Dy, W. Tam, and K. L. Beemon Reticuloendotheliosis Virus Strain T Induces miR-155, Which Targets JARID2 and Promotes Cell Survival J. Virol., December 1, 2009; 83(23): 12009 - 12017. [Abstract] [Full Text] [PDF] J. Liu, N. Bandyopadhyay, S. Ranka, M. Baudis, and T. Kahveci Inferring progression models for CGH data Bioinformatics, September 1, 2009; 25(17): 2208 - 2215. [Abstract] [Full Text] [PDF] S. Hartmann, J. I. Martin-Subero, S. Gesk, J. Husken, M. Giefing, I. Nagel, J. Riemke, A. Chott, W. Klapper, M. Parrens, et al. 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