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Prepublished online as a Blood First Edition Paper on November 27, 2002; DOI 10.1182/blood-2002-08-2464.
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Blood, 1 April 2003, Vol. 101, No. 7, pp. 2789-2796
NEOPLASIA
High-level expression of BCL3 differentiates
t(2;5)(p23;q35)-positive anaplastic large cell lymphoma from
Hodgkin disease
Momoko Nishikori,
Yoshitomo Maesako,
Chiyoko Ueda,
Masayuki Kurata,
Takashi Uchiyama, and
Hitoshi Ohno
From the Department of Hematology and Oncology,
Graduate School of Medicine, Kyoto University, Japan.
Anaplastic large cell lymphoma (ALCL) with t(2;5)(p23;q35) and
Hodgkin disease (HD) share many cellular features, including expression
of CD30. We compared gene expression profiles of 4 ALCL (Karpas 299, SU-DHL-1, DEL, SR-786) and 3 HD cell lines and found that
BCL3, which encodes a nuclear protein belonging to the
I B family of inhibitors of nuclear factor-B (NF-B)
transcriptional factors, was expressed at higher levels in ALCL than
HD. Northern and Western blotting analyses confirmed the high-level
expression of BCL3 in ALCL at both mRNA and protein levels.
We established a real-time reverse transcriptase-mediated polymerase
chain reaction assay to measure the BCL3 mRNA level and
found a predominant level of BCL3 expression in
t(2;5)+ ALCL; the levels of cell lines and clinical
materials were comparable to or higher than that of a B-cell chronic
lymphocytic leukemia carrying t(14;19)(q32;q13). Southern blotting and
fluorescence in situ hybridization disclosed that the BCL3
gene copies were amplified in SU-DHL-1, whereas Karpas 299 carried 4 BCL3 gene loci. The BCL3 gene
contains 2 cytosine-guanine dinucleotide (CpG) islands, and
the intragenic 3' CpG was entirely demethylated in SU-DHL-1 and DEL. In
contrast to HD, in which NF-B was constitutively activated, ALCL
cells consistently showed (p50)2 homodimer binding activity
on electrophoretic mobility shift assay. It is suggested that the
high-level nuclear Bcl-3 sequestrates the (p50)2 homodimer to the nucleus, which may account for the contradictory effect of CD30
stimulation on ALCL and HD. We propose that BCL3 is
overexpressed by genetic and epigenetic modifications, potentially
contributing to the development of t(2;5)+ ALCL.
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