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[Cancer Research 60, 549-552, February 1, 2000]
© 2000 American Association for Cancer Research

Advances in Brief

Genomic Imbalances Including Amplification of the Tyrosine Kinase Gene JAK2 in CD30+ Hodgkin Cells1

Stefan Joos2, Manfred Küpper, Sibylle Ohl, Frederike von Bonin, Gunhild Mechtersheimer, Martin Bentz, Peter Marynen, Peter Möller, Michael Pfreundschuh, Lorenz Trümper and Peter Lichter

Deutsches Krebsforschungszentrum, Abteilung Organisation Komplexer Genome (H0700), D-69120 Heidelberg [S. J., M. K., S. O., P. L.]; Universitätskliniken des Saarlandes, Innere Medizin I, D-66421 Homburg/Saar [F. v. B., M. P., L. T.]; Pathologisches Institut, Universität Heidelberg, D-69120 Heidelberg [G. M.]; Abteilung Innere Medizin III, D-89081 Ulm [M. B.]; Human Genome Laboratory, B-3000 Leuven [P. Ma.]; Abteilung für Pathologie des Universitätsklinikums Ulm, D-89081 Ulm [P. Mö.], Germany

Comparative genomic hybridization was applied for a comprehensive screening of frequently occurring net gains and losses of chromosomal subregions in small populations of CD30+ Hodgkin cells and their morphological variants. In 12 Hodgkin’s lymphomas, recurrent gains were detected on chromosomal arms 2p, 9p, and 12q (in six, four, and five tumors, respectively) and distinct high-level amplifications were identified on chromosomal bands 4p16, 4q23-q24, and 9p23-p24. In Hodgkin cells with 9p23-p24 amplification, fluorescence in situ hybridization revealed an increased copy number of chromosomal sequences spanning the tyrosine kinase gene JAK2. Several of the imbalances described, in particular a gain in chromosomal arm 9p that includes JAK2 amplification, are similar to the genomic changes detected in primary mediastinal B-cell lymphoma.




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