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Cloning of the ALL-1 Fusion Partner, the AF-6 Gene, Involved in Acute Myeloid Leukemias with the t(6;11) Chromosome Translocation¹

Jefferson Cancer Institute, Jefferson Cancer Center and Department of Microbiology and Immunology, Jefferson Medical College of Thomas Jefferson University, Philadelphia, Pennsylvania 19107 [R. P., Y. G., H. A., T. N., O. C., H. S., K. H., C. M. C., E. C.]; University of California Medical Center, Los Angeles, California 90024 [R. P. G.]; University of Pennsylvania, Philadelphia, Pennsylvania 19104 [P. C. N.]; and Nagasaki University School of Medicine, Nagasaki 852, Japan [K. K., Y. M.]

² To whom requests for reprints should be addressed.

Reciprocal chromosome translocations involving 11q23 are frequently associated with acute leukemias, with the t(4;11) translocation predominating among acute lymphoblastic leukemias, and the t(9;11), t(11;19) and t(6;11) translocations most common among acute myeloid leukemias. In each of these translocations the ALL-1 gene, located at 11q23 and constituting the human homologue of Drosophila trithorax, fuses to a specific gene on the partner chromosome to produce a chimeric protein. Here we report the cloning and the characterization of the partner gene from chromosome 6 (AF-6). AF-6 is expressed in a variety of cell types and encodes a protein of 1612 amino acids. The protein contains short stretches rich in prolines, charged amino acids, serines, or glutamines. In addition, the AF-6 protein contains the GLGF motif shared with several proteins of vertebrates and invertebrates thought to be involved in signal transduction at special cell-cell junctions.

¹ Supported by grants from the National Cancer Institute (CA39860) and from the Falk Medical Research Trust; Genbank accession number is U02478.

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 10/ 4/93. Accepted 10/28/93.

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