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Division of Oncology, Department of Pediatrics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104 [C. A. F., B. J. L.]; Center for Cancer and Blood Disorders, Children's Medical Center of Dallas, University of Texas Southwestern Medical Center, Dallas, Texas 75235 [N. J. W.]; Thomas Jefferson University Cancer Research Center, Philadelphia, Pennsylvania 19107 [M. N., C. M. C.]; and Department of Pediatrics, Cook-Fort Worth Children's Medical Center, Fort Worth, Texas 76104 [W. P. B.]
Translocations at chromosomal band 11q23 characterize most de novo acute lymphoblastic leukemias (ALL) of infants, acute myeloid leukemias (AML) of infants and young children, and secondary AMLs following epipodophyllotoxin exposure. The chromosomal breakpoints at 11q23 have been cloned from isolated cases of de novo ALL and AML. Using an 859-base pair BamHI fragment of human ALL-1 complementary DNA that recognizes the genomic breakpoint region for de novo ALL and AML, we investigated two cases of secondary AML that followed etoposidetreated primary B-lineage ALL. In the first case, the translocation occurred between chromosomes 9 and 11 and the breakpoint at 11q23 localized to the same 9-kilobase region of the ALL-1 gene that is disrupted in most of the de novo leukemias. In the second case the translocation was between chromosomes 11 and 19. The breakpoint occurred outside of the ALL-1 breakpoint cluster region.
1 To whom requests for reprints should be addressed, at Division of Oncology, Department of Pediatrics, Room 9093, Children's Hospital of Philadelphia, 34th St. and Civic Center Blvd., Philadelphia, PA 19104.
Received 4/12/93. Accepted 5/12/93.
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