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Papers In Press, published online ahead of print September 12, 2002
Biology Division, National Cancer Center Research Institute, Tokyo 104-0045
Corresponding Author: jyokota{at}gan2.ncc.go.jp
To understand molecular pathways underlying 9p21 deletions, which lead to inactivation of the p16/CDKN2A, p14/ARF and/or p15/CDKN2B genes, in lymphoid leukemia, 30 breakpoints were cloned from 15 lymphoid leukemia cell lines. Seventeen (57 %) breakpoints were mapped at 5 breakpoint cluster sites, BCS-LL1 to LL5, each of <15-bp in size. Two breakpoint cluster sites were located within the ARF and CDKN2B loci, respectively, while the remaining three were located >100-kb distal to the CDKN2A, ARF and CDKN2B loci. The sequences of breakpoint junctions indicated that deletions in the 11 (73 %) cell lines were mediated by illegitimate V(D)J recombination targeted at the 5 BCS-LL and 6 other sites, which contain sequences similar to recombination signal sequences for V(D)J recombination. An extrachromosomal V(D)J recombination assay indicated that BCS-LL3, at which the largest number of breakpoints (i.e., 5 breakpoints) was clustered, has a V(D)J recombination potential 150-fold less than the consensus recombination signal sequence. Three other BCS-LLs tested also showed V(D)J recombination potential, although it was lower than that of BCS-LL3. These results indicated that illegitimate V(D)J recombination, that was targeted at several ectopic recombination signal sequences widely distributed in 9p21, caused a large fraction of 9p21 deletions in lymphoid leukemia.
J. Biol. Chem, 10.1074/jbc.M208353200
Submitted on August 15, 2002
Revised on September 12, 2002
Accepted on September 12, 2002
Prevalent involvement of illegitimate V(D)J recombination in chromosome 9p21 deletions in Lymphoid Leukemia
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