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Blood, 1 August 2004, Vol. 104, No. 3, pp. 795-801.
Prepublished online as a Blood First Edition Paper on April 13, 2004; DOI 10.1182/blood-2003-12-4175.
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NEOPLASIA
Genomic DNA-chip hybridization in t(11;14)-positive mantle cell lymphomas shows a high frequency of aberrations and allows a refined characterization of consensus regions
Holger Kohlhammer,
Carsten Schwaenen,
Swen Wessendorf,
Karlheinz Holzmann,
Hans A. Kestler,
Dirk Kienle,
Thomas F. E. Barth,
Peter Möller,
German Ott,
Jörg Kalla,
Bernhard Radlwimmer,
Armin Pscherer,
Stephan Stilgenbauer,
Hartmut Döhner,
Peter Lichter, and
Martin Bentz
From the Departments of Innere Medizin I and Innere Medizin III, Medizinische Klinik der Universität Ulm, Ulm, Germany; Departments of Neuroinformatik and Pathologie, Universität Ulm, Ulm, Germany; Department of Pathologie, Universität Würzburg, Würzburg, Germany; and Department of Molekulare Genetik, Deutsches Krebsforschungszentrum, Heidelberg, Germany.
Tumor samples of 53 patients with t(11;14)-positive mantle cell lymphomas (MCLs) were analyzed by matrix-based comparative genomic hybridization (matrix-CGH) using a dedicated DNA array. In 49 cases, genomic aberrations were identified. In comparison to chromosomal CGH, a 50% higher number of aberrations was found and the high specificity of matrix-CGH was demonstrated by fluorescence in situ hybridization (FISH) analyses. The 11q gains and 13q34 deletions, which have not been described as frequent genomic aberrations in MCL, were identified by matrix-CGH in 15 and 26 cases, respectively. For several genomic aberrations, novel consensus regions were defined: 8p21 (size of the consensus region, 2.4 megabase pairs [Mbp]; candidate genes: TNFRSF10B, TNFRSF10C, TNFRSF10D); 10p13 (2.7 Mbp; BMI1); 11q13 (1.4 Mbp; RELA); 11q13 (5.2 Mbp; CCND1); 13q14 (0.4 Mbp; RFP2, BCMSUN) and 13q34 (6.9 Mbp). In univariate analyses correlating genomic aberrations and clinical course, 8p- and 13q14- deletions were associated with an inferior overall survival. These data provide a basis for further studies focusing on the identification of pathogenetically or clinically relevant genes in MCL.
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