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Blood, 15 January 2001, Vol. 97, No. 2, pp. 509-515
NEOPLASIA
Role for CCG-trinucleotide repeats in the pathogenesis of chronic
lymphocytic leukemia
Rebecca L. Auer,
Christopher Jones,
Roman A. Mullenbach,
Denise Syndercombe-Court,
Donald W. Milligan,
Christopher D. Fegan, and
Finbarr E. Cotter
From the Department of Experimental Haematology, St
Bartholomew's, and The Royal London School of Medicine and Dentistry,
London; and the Department of Haematology, Birmingham Heartlands
Hospital, Birmingham, United Kingdom.
Chromosome 11q deletions are frequently observed in chronic
lymphocytic leukemia (CLL) in association with progressive disease and
a poor prognosis. A minimal region of deletion has been assigned to
11q22-q23. Trinucleotide repeats have been associated with anticipation
in disease, and evidence of anticipation has been observed in various
malignancies including CLL. Loss of heterozygosity at 11q22-23 is
common in a wide range of cancers, suggesting this is an unstable area
prone to chromosome breakage. The location of 8 CCG-trinucleotide
repeats on 11q was determined by Southern blot analysis of a 40-Mb YAC
and PAC contig spanning 11q22-qter. Deletion breakpoints in CLL are
found to co-localize at specific sites on 11q where CCG repeats are
located. In addition, a CCG repeat has been identified within the
minimal region of deletion. Specific alleles of this repeat are
associated with worse prognosis. Folate-sensitive fragile sites are
regions of late replication and are characterized by CCG repeats. The
mechanism for chromosome deletion at 11q could be explained by a delay
in replication. Described here is an association between CCG repeats
and chromosome loss suggesting that in vivo "fragile sites" exist
on 11q and that the instability of CCG repeats may play an important
role in the pathogenesis of CLL.
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