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Rearrangements of the MLL gene in therapy-related acute myeloid leukemia in
patients previously treated with agents targeting DNA- topoisomerase II
HJ Super, NR McCabe, MJ Thirman, RA Larson, MM Le Beau, J Pedersen-Bjergaard, P Philip, MO Diaz and JD Rowley
Department of Molecular Genetics and cell Biology, University of Chicago,
IL 60637.
Chromosome band 11q23 is frequently involved in acute myeloid leukemia
(AML) and acute lymphoblastic leukemia (ALL) de novo, as well as in
myelodysplastic syndromes (MDS) and lymphoma. Five percent to 15% of
patients treated with chemotherapy for a primary neoplasm develop
therapy-related AML (t-AML) that may show rearrangements, usually
translocations involving band 11q23 or, less often, 21q22. These leukemias
develop after a relatively short latent period and often follow the use of
drugs that inhibit the activity of DNA-topoisomerase II (topo II). We
previously identified a gene, MLL (myeloid-lymphoid leukemia or
mixed-lineage leukemia), at 11q23 that is involved in the de novo
leukemias. We have studied 17 patients with t-MDS/t-AML, 12 of whom had
cytogenetically detectable 11q23 rearrangements. Ten of the 12 t-AML
patients had received topo II inhibitors and 9 of these, all with balanced
translocations of 11q23, had MLL rearrangements on Southern blot analysis.
None of the patients who had not received topo II inhibitors showed an MLL
rearrangement. Of the 5 patients lacking 11q23 rearrangements, some of whom
had monoblastic features, none had an MLL rearrangement, although 4 had
received topo II inhibitors. Our study indicates that the MLL gene
rearrangements are similar both in AML that develops de novo and in t-AML.
The association of exposure to topo II- reactive chemotherapy with 11q23
rearrangements involving the MLL gene in t-AML suggests that topo II may
play a role in the aberrant recombination events that occur in this region
both in AML de novo and in t-AML.
Volume 82,
Issue 12,
pp. 3705-3711,
12/15/1993
Copyright © 1993 by The American Society of Hematology
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