Potential topoisomerase II DNA-binding sites at the breakpoints of a t(9;11) chromosome translocation in acute myeloid leukemia

We have examined a t(9;11)(p22;q23) chromosome translocation in an acute myeloid leukemia of an infant. The breakpoints on the two chromosomes occurred within introns of the involved genes: AF-9 on chromosome 9, and ALL-1 on chromosome 11. Sequence analysis identified heptamers flanking the breakpoi...

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Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 1993-10, Vol.53 (19), p.4489-4492
Main Authors: NEGRINI, M, FELIX, C. A, MARTIN, C, LANGE, B. J, NAKAMURA, T, CANAANI, E, CROCE, C. M
Format: Article
Language:English
Subjects:
Amino Acid Sequence
Base Sequence
Binding Sites
Biological and medical sciences
Blotting, Southern
Chromosomes, Human, Pair 11
Chromosomes, Human, Pair 9
DNA Nucleotidyltransferases - metabolism
DNA Topoisomerases, Type II - metabolism
DNA, Neoplasm - metabolism
Hematologic and hematopoietic diseases
Humans
Introns
Leukemia, Myeloid, Acute - genetics
Leukemia, Myeloid, Acute - metabolism
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
Medical sciences
Molecular Sequence Data
Restriction Mapping
Sequence Homology, Nucleic Acid
Translocation, Genetic
VDJ Recombinases
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Summary:We have examined a t(9;11)(p22;q23) chromosome translocation in an acute myeloid leukemia of an infant. The breakpoints on the two chromosomes occurred within introns of the involved genes: AF-9 on chromosome 9, and ALL-1 on chromosome 11. Sequence analysis identified heptamers flanking the breakpoints on both chromosomes 9 and 11, suggesting that the V-D-J recombinase was involved in the translocation. The presence of an N-region between the two chromosomes supports the hypothesis that a mistake in V-D-J joining was involved in the genesis of the translocation and indicates that terminal deoxynucleotidyl transferase was expressed in the cells from which this acute myeloid leukemia originated. In addition, potential topoisomerase II DNA-binding sites were found near the breakpoints of both chromosomes, suggesting the involvement of altered topoisomerase II activity in this translocation. Altered topoisomerase II activity in the presence of an active V-D-J recombinase may be a pathogenetic mechanism of acute myeloid leukemia with rearrangements at 11q23.
ISSN:0008-5472
1538-7445