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Molecular cloning of complex chromosomal translocation
t(8;14;12)(q24.1;q32.3;q24.1) in a Burkitt lymphoma cell line defines a new
gene (BCL7A) with homology to caldesmon
VJ Zani, N Asou, D Jadayel, JM Heward, J Shipley, E Nacheva, K Takasuki, D Catovsky and MJ Dyer
Academic Department of Haematology and Cytogenetics, Institute of Cancer
Research-Royal Marsden Hospital, Sutton, Surrey, UK.
Chromosome 12q24.1 is a recurrent breakpoint in high-grade B-cell non-
Hodgkin lymphoma (B-NHL). To identify the genes involved at 12q24.1,
molecular cloning of a three-way translocation
t(8;14;12)(q24.1;q32.3;q24.1) in a Burkitt lymphoma cell line (Wien 133)
was performed; all four translocation breakpoints were cloned and
sequenced. Analysis of clones encompassing the der(12)(12;14)(q24.1;q32.3)
breakpoint showed a CpG island from chromosome 12q24.1 juxtaposed in a
tail-to-tail configuration with a productively rearranged Ig VH4-DH-JH5
gene. A total of 4.5 kb of genomic DNA including the CpG island was
sequenced and analyzed using gene-identification programs; all three
programs identified a potential 92-bp exon within the centromeric boundary
of the CpG island. Using this as a probe, an RNA transcript of 3.8 kb,
expressed at low levels in a wide variety of normal tissues, was detected.
Overlapping cDNA clones were isolated and sequenced. The longest
open-reading frame predicted a serine-rich protein of 231 amino acids. This
protein, termed BCL7A, exhibited no recognizable protein motifs but showed
homology with the actin-binding protein, caldesmon. In Wien 133, the BCL7A
breakpoint occurred within the first intron and resulted in a MYC- BCL7A
fusion transcript, with exon I of BCL7A being replaced by MYC exon I. The
normal, untranslocated allele of BCL7A was also expressed without mutation.
One of the 11 other B-NHL cell lines examined with 12q24.1 cytogenetic
abnormalities, a mediastinal B-NHL cell line (Karpas 1106), showed
biallelic rearrangement within the first intron of BCL7A, which was
adjacent to the breakpoint observed in Wien 133. Disruption of the
amino-terminus of BCL7A defines a new mechanism in the pathogenesis of a
subset of high-grade B-NHL.
Volume 87,
Issue 8,
pp. 3124-3134,
04/15/1996
Copyright © 1996 by The American Society of Hematology
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