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Blood, 1 December 2001, Vol. 98, No. 12, pp. 3413-3420
NEOPLASIA
The BCL11 gene family:
involvement of BCL11A in lymphoid
malignancies
Ed Satterwhite,
Takashi Sonoki,
Tony G. Willis,
Lana Harder,
Rachael Nowak,
Emma L. Arriola,
Hui Liu,
Helen P. Price,
Stefan Gesk,
Doris Steinemann,
Brigitte Schlegelberger,
David G. Oscier,
Reiner Siebert,
Philip W. Tucker, and
Martin J. S. Dyer
From the Academic Department of Haematology and
Cytogenetics, Haddow Laboratories, Institute of Cancer Research,
Sutton, United Kingdom; University of Texas at Austin,
Institute for Cellular and Molecular Biology, Molecular Genetics and
Microbiology, Austin, TX; Institute of Human Genetics, University
Hospital Kiel, Kiel, Germany; Department of Haematology,
Royal Bournemouth Hospital, Bournemouth, United Kingdom.
Many malignancies of mature B cells are characterized by
chromosomal translocations involving the immunoglobulin heavy chain (IGH) locus on chromosome 14q32.3 and result in deregulated
expression of the translocated oncogene. t(2;14)(p13;q32.3) is a rare
event in B-cell malignancies. In contrast, gains and amplifications of
the same region of chromosome 2p13 have been reported in 20% of
extranodal B-cell non-Hodgkin lymphomas (B-NHL), in follicular and
mediastinal B-NHL, and in Hodgkin disease (HD). It has been suggested
that REL, an NF- B gene family member, mapping within the
amplified region, is the pathologic target. However, by molecular cloning of t(2;14)(p13;q32.3) from 3 cases of aggressive B-cell chronic
lymphocytic leukemia (CLL)/immunocytoma, this study has shown clustered
breakpoints on chromosome 2p13 immediately upstream of a CpG island
located about 300 kb telomeric of REL. This CpG island was
associated with a Krüppel zinc finger gene (BCL11A), which is normally expressed at high levels only in fetal brain and in
germinal center B-cells. There were 3 major RNA isoforms of
BCL11A, differing in the number of carboxy-terminal zinc
fingers. All 3 RNA isoforms were deregulated as a consequence of
t(2;14)(p13;q32.3). BCL11A was highly conserved, being
95% identical to mouse, chicken, and Xenopus homologues.
BCL11A was also highly homologous to another gene
(BCL11B) on chromosome 14q32.1. BCL11A
coamplified with REL in B-NHL cases and HD lymphoma cell
lines with gains and amplifications of 2p13, suggesting that
BCL11A may be involved in lymphoid malignancies through
either chromosomal translocation or amplification.
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