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Blood, 15 February 2002, Vol. 99, No. 4, pp. 1474-1477
BRIEF REPORT
Recurrent involvement of the REL and BCL11A
loci in classical Hodgkin lymphoma
José I. Martín-Subero,
Stefan Gesk,
Lana Harder,
Takashi Sonoki,
Philip W. Tucker,
Brigitte Schlegelberger,
Werner Grote,
Francisco J. Novo,
María J. Calasanz,
Martin L. Hansmann,
Martin J. S. Dyer, and
Reiner Siebert
From the Institute of Human Genetics, University
Hospital Kiel, Germany; Department of Genetics, University of Navarra,
Pamplona, Spain; Internal Medicine II, Kumamoto University School of
Medicine, Japan; Institute for Cellular and Molecular Biology,
University of Texas at Austin; Department of Pathology, University of
Frankfurt, Germany; and Department of Haematology, University of
Leicester, United Kingdom.
Comparative genomic hybridization studies have shown gains in
chromosome region 2p as the most common imbalance in classical Hodgkin
lymphoma (cHL). The minimal region of gain contained 2 candidate
oncogenes, REL and BCL11A. This study examined
the involvement of REL and BCL11A loci in 44 primary cases of cHL by combined immunophenotyping and interphase
cytogenetics (FICTION). A median 2p13 copy number above the
tetraploid range was detected in 24 (55%) cases. Adjustment for
centromere 2 copy number indicated gains of 2p13 in 11 of 31 cHLs
(35%) with 8 (26%) high-level amplifications. One cHL displayed
selective amplification of the REL locus not affecting
BCL11A; another case studied by FICTION and a cHL with cytogenetic 2p change investigated by fluorescence in situ
hybridization showed signal patterns suggesting breakpoints in the
region spanned by the REL probe. These data indicate that
REL rather than BCL11A may be the target of the
2p13 alterations in cHL.

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