Human Molecular Genetics, Vol 7, 767-776, Copyright © 1998 by Oxford University Press
AR Jeffs, SM Benjes, TL Smith, SJ Sowerby and CM Morris
Chronic myeloid leukaemia (CML) develops when two genes, BCR on chromosome
22 and ABL on chromosome 9, recombine to form a hybrid BCR- ABL gene with
leukaemogenic properties. The mechanism which underlies this recombination
is unknown, but additional chromosome sites may be involved to form complex
BCR-ABL rearrangements. The majority of breakpoints in BCR occur within a 5
kb major breakpoint cluster region, M-Bcr. Here, we show that the 3' part
of M-Bcr recombined within, or immediately adjacent to, Alu elements at the
additional sites in all five complex BCR-ABL rearrangements that have been
examined so far. This is a new finding which suggests that Alu sequences
have an affinity for the BCR-ABL recombination process in complex
rearrangements, and provides additional evidence for the association of
these elements with somatic rearrangements which cause human leukaemia. We
further show that sequence motifs similar to IgH switch pentamers and
consensus binding sites of the lymphoid-associated Translin protein are
present on one or more participating strands at 3'M-Bcr recombination
sites. Motifs similar to Translin-binding sites were also identified within
the Alu consensus. Expressed sequences mapped close to the breakpoint sites
on other chromosomes in three of the five cases examined.
ARTICLES
The BCR gene recombines preferentially with Alu elements in complex BCR- ABL translocations of chronic myeloid leukaemia
Cytogenetic and Molecular Oncology Unit, Department of Pathology, PO Box 4345, Christchurch School of Medicine, Christchurch, New Zealand.
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