RT Journal Article
SR Electronic
T1 Genomic Imbalances Including Amplification of the Tyrosine Kinase Gene <em>JAK2</em> in CD30<sup>+</sup> Hodgkin Cells
JF Cancer Research
JO Cancer Res
FD American Association for Cancer Research
SP 549
OP 552
VO 60
IS 3
A1 Joos, Stefan
A1 Küpper, Manfred
A1 Ohl, Sibylle
A1 von Bonin, Frederike
A1 Mechtersheimer, Gunhild
A1 Bentz, Martin
A1 Marynen, Peter
A1 Möller, Peter
A1 Pfreundschuh, Michael
A1 Trümper, Lorenz
A1 Lichter, Peter
YR 2000
UL http://cancerres.aacrjournals.org/content/60/3/549.abstract
AB 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.