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Site-specific DNA cleavage within the MLL breakpoint cluster region induced
by topoisomerase II inhibitors [see comments]
PD Aplan, DS Chervinsky, M Stanulla and WC Burhans
Department of Molecular Medicine and Pedriatrics, Roswell Park Cancer
Institute, Buffalo, NY 14263, USA.
The MLL gene located at 11q23 is frequently disrupted by chromosomal
translocation in a wide spectrum of newly diagnosed acute leukemias.
Recently, it has become apparent that the MLL gene is very frequently
disrupted by chromosomal translocations in patients with secondary
leukemias associated with chemotherapeutic regimens incorporating
topoisomerase II inhibitors. These secondary leukemias associated with
topoisomerase II inhibitors (most commonly teniposide, etoposide, or
doxorubicin) have distinct clinical and biologic features which have led to
the speculation that they are induced by treatment with topoisomerase II
inhibitors. We have identified a site within the MLL breakpoint cluster
region (bcr) that is highly sensitive to double- strand DNA cleavage
induced by topoisomerase II inhibitors. This finding is quite specific and
highly reproducible. Although it was initially discovered in malignant
lymphoblasts isolated from a patient receiving multiagent chemotherapy,
this site-specific double-strand DNA cleavage can be induced in tissue
culture using malignant cell lines as well as peripheral blood from normal
individuals. Site-specific cleavage occurs in a significant fraction of
cells using a variety of model systems, is both time and dose dependent,
and can be induced with either doxorubicin or etoposide. This site-specific
cleavage maps to the same region as a consensus topoisomerase II cleavage
site within the MLL bcr. These results suggest that site specific cleavage
within the MLL bcr induced by topoisomerase II inhibitors may be an early
step leading to MLL translocations and secondary leukemia.
Volume 87,
Issue 7,
pp. 2649-2658,
04/01/1996
Copyright © 1996 by The American Society of Hematology
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