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Prepublished online as a Blood First Edition Paper on January 2, 2003; DOI 10.1182/blood-2002-08-2577. This Article Full Text (PDF) All Versions of this Article: 2002-08-2577v1 101/9/3681    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 Barth, T. F E Articles by Moeller, P. Search for Related Content PubMed PubMed Citation Articles by Barth, T. F E Articles by Moeller, P. Social Bookmarking                   What's this? Submitted August 22, 2002 Accepted December 23, 2002 Gains of 2p involving the REL locus correlate with nuclear c-Rel protein accumulation in neoplastic cells of classical Hodgkin's lymphoma Thomas F E Barth*, Jose I Martin-Subero, Stefan Joos, Christiane K Menz, Cornelia Hasel, Gunhild Mechtersheimer, Reza M Parwaresch, Peter Lichter, Reiner Siebert, and Peter Moeller Institut fuer Pathologie, Universitaet Ulm, Ulm, Germany Institut fuer Humangenetik, Universitaetsklinikum Kiel, Kiel, Germany Abteilung Organisation komplexer Genome, Deutsches Krebsforschungszentrum, Heidelberg, Germany Institut fuer Pathologie, Universitaet Heidelberg, Heidelberg, Germany Institut fuer Haematopathologie, Universitaetsklinikum Kiel, Kiel, Germany * Corresponding author; email: thomas.barth{at}medizin.uni-ulm.de. Structural aberrations of the short arm of chromosome 2 mostly resulting in gain of 2p13~16 have recently been described as being highly recurrent in Hodgkin/Reed-Sternberg (HRS) cells of classical Hodgkin's lymphoma (cHL). As these gains consistently lead to increased copy numbers of the REL oncogene locus, we investigated the expression of the c-Rel protein in a series of 30 cHL cases with known genomic REL status as determined by comparative genomic hybridization and interphase cytogenetics. Expression of the c-Rel protein was investigated in 26 biopsies by immunohistochemistry. Distinct patterns were observed in HRS cells with no staining, cytoplasmic, and/or nuclear staining for c-Rel. All 13 samples with additional copies of the REL locus displayed nuclear staining for c-Rel while 13 cHL lacking 2p gains displayed a significantly lower proportion or complete absence of HRS cells with nuclear c-Rel expression. Detailed analysis using combined immunophenotyping and interphase cytogenetics of individual HRS cells demonstrated that REL gains correlated with the presence of nuclear c-Rel staining. Additionally, in two cHL with translocation breakpoints in 2p13~16, nuclear staining of c-Rel was observed, in one of them with a staining pattern indicative of a truncated c-Rel protein. The correlation between structural aberrations involving the REL locus and nuclear c-Rel accumulation in HRS cells qualifies REL as a target gene of the frequent gains in 2p in cHL. The data suggest that REL aberrations are a genetic mechanism contributing to constitutive NF-B/Rel activation in cHL. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. Dutta, G. Fan, and C. Gelinas CAPER{alpha} Is a Novel Rel-TAD-Interacting Factor That Inhibits Lymphocyte Transformation by the Potent Rel/NF-{kappa}B Oncoprotein v-Rel J. 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