Co-Authors:
Fainstein, E., Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel
Marcelle, C., Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel
Rosner, A., Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel
Canaani, E., Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel
Gale, R.P., Department of Medicine, University of California, Los Angeles, CA 90024, United States
Dreazen, O., Department of Medicine, University of California, Los Angeles, CA 90024, United States
Smith, S.D., Department of Pediatrics, Children's Hospital at Stanford, Palo Alto, CA 94304, United States
Croce, C.M., Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, United States
Abstract:
The leukaemic cells of more than 90% of chronic myelogenous leukaemia (CML) patients and of 10% of acute lymphocytic leukaemia (ALL) patients carry the t(9:22) (q34:qll) translocation which generates the Philadelphia chromosome (Ph1). In CML the abl gene is translocated from chromosome 9 to the centre of the bcr gene on chromosome 22 and this results in production of chimaeric bcr-abl RNA translated into a protein of relative molecular mass (Mr) 210,000 (210K). Our data indicate that in ALL abl is translocated into the 5' region of the bcr gene. The consequence of this is the expression of a fused transcript in which the first exon of bcr is linked to the second abl exon. This transcript encodes a 190K protein kinase. © 1987 Nature Publishing Group.