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Division of Oncology, Department of Pediatrics, Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104 [C. A. F., B. J. L., M. R. H.], and Department of Biochemistry, Thomas Jefferson University Medical College, Philadelphia, Pennsylvania 19107 [J. F., M-A. B.]
Human leukemias with 11q23 translocations occur sporadically and after cancer treatment with DNA topoisomerase II-targeted drugs. To investigate this process, we examined DNA topoisomerase II cleavage in vitro in subclones of the normal 11q23 genomic homologue and a t(9;11) translocation breakpoint junction. Cleavage was assayed with limiting dilutions of enzyme in the presence or absence of epipodophyllotoxin and ATP. The strongest sites of cleavage coincided with the t(9;11) breakpoint site and two other translocation breakpoint sites within the normal homologue. These results support the involvement of DNA topoisomerase II in the translocation process at chromosome band 11q23.
1 This work was supported by a Leukemia Society of America Special Fellow Award and American Cancer Society Grant DHP-143 (to C. A. F.), and NIH Grant CA58755 (to M. A. B.).
2 To whom requests for reprints should be addressed, at Division of Oncology, Room 902, Leonard and Madlyn Abramson Pediatric Research Building, Children's Hospital of Philadelphia, 324 South 34th Street, Philadelphia, PA 19104.
Received 6/19/95. Accepted 8/18/95.
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