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Division of Hematologic Oncology and Bone Marrow Transplantation [M. A. C., G. P. H., M. P. S., S. R. F., K. M., M. R. B., C. D. B.]; Division of Molecular Medicine [M. A. C.], Cytogenetics Research Laboratory [K. M., C. D. B.], Molecular Immunology [M. P S.], and Pathology [M. B.], Department of Medicine, Roswell Park Cancer Institute, Buffalo, New York 14263, and Jefferson Cancer Institute and Department of Microbiology and Immunology, Jefferson Medical College of Thomas Jefferson University, Philadelphia, Pennsylvania 19104 [S. A. S., C. M. C.]
2 To whom requests for reprints should be addressed.
Translocations which involve chromosome band 11q23 are frequently found in infants and adults with acute myeloid leukemia (AML) or acute lymphoblastic leukemia. We previously cloned a gene called ALL-1 which spans the 11q23 breakpoint and is rearranged in most cases of leukemia with 11q23 abnormalities. In the present report, we have investigated the occurrence of ALL-1 rearrangement in cases of AML without cytogenetic evidence of 11q23 abnormalities. We detected molecular rearrangements of the ALL-1 gene in 3 of 4 patients with de novo AML and trisomy 11 as a sole chromosomal abnormality. Furthermore, we found DNA rearrangements of ALL-1 in 2 of 19 patients with de novo AML and normal cytogenetics. We conclude that molecular rearrangement of ALL-1 often can be detected in de novo AML, despite the absence of cytogenetic abnormalities involving 11q23.
1 Supported by an Outstanding Investigator Grant (CA39860) to C. M. C. from the National Cancer Institute and by National Cancer Institute Grants CA01752 and CA37027 and the Coleman Leukemia Research Fund.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 11/11/93. Accepted 12/ 6/93.
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