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ALL-1 gene rearrangements in DNA topoisomerase II inhibitor-related
leukemia in children
CA Felix, MR Hosler, NJ Winick, M Masterson, AE Wilson and BJ Lange
Department of Pediatrics, Children's Hospital of Philadelphia, University
of Pennsylvania School of Medicine 19104, USA.
We examined clinical, morphologic, and cytogenetic features and ALL-1 (MLL,
Htrxl, HRX) gene rearrangements in 17 cases of secondary leukemia that
occurred 11 months to 9 years from diagnoses of primary cancers in children
who received topoisomerase II inhibitors or developed secondary leukemias
typical of those associated with this therapy. Primary diagnoses included
nine solid tumors and eight leukemias. Ten secondary leukemias were acute
myeloid leukemia (AML), one was of mixed lineage, two were acute
lymphoblastic leukemia (ALL), and four presented as myelodysplasia. Of 15
cases with 11q23 involvement, 11 (73%) were cytogenetically identifiable;
four cases had molecular rearrangement only. By Southern blot,
rearrangements within the ALL-1 gene were similar to sporadic cases. The
results of this analysis suggest the following: (1) In most pediatric cases
of topoisomerase II inhibitor-associated leukemia, there is disruption of
the breakpoint cluster region of the ALL-1 gene at chromosomal band 11q23.
(2) Exposure histories vary in secondary 11q23 leukemia, as the only
topoisomerase II inhibitor was dactinomycin in one case, and, in another
case, no topoisomerase II inhibitor was administered. (3) There is
clinical, morphologic, cytogenetic, and molecular heterogeneity in
pediatric secondary 11q23 leukemia. (4) There are some survivors of
pediatric secondary 11q23 leukemia, but the outcome is most often fatal.
Volume 85,
Issue 11,
pp. 3250-3256,
06/01/1995
Copyright © 1995 by The American Society of Hematology
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