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Leukaemia Research Fund Centre at the Institute of Cancer Research, Fulham Road, Chester Beatty Laboratories, London, SW3 6JB, United Kingdom [P. P., S. A. R., C. A. B., L. M. W.], and Heinrich-Pette-Institut für Experimentelle Virologie und Immunologie an der Universität, Hamburg, Germany [P. P., C. S.]
In human leukemia, activation of the ABL proto-oncogene locus on chromosome 9 most commonly occurs as a result of its fusion to the BCR locus on chromosome 22. The resulting chimeric protein displays an elevated tyrosine kinase activity. We have identified a novel activation of ABL which involves a gene located on chromosome 12, designated TEL. Like BCR, TEL is fused in-frame with ABL and produces a fusion protein with an elevated tyrosine kinase activity when assayed in an immune complex. The amino-terminal sequences of TEL encode a helix-loop-helix motif which may mediate dimerization.
1 This work was supported by the Leukaemia Research Fund of Great Britain and the Deutsche Krebshilfe.
2 Present address: Genetics Unit, Department of Anatomy, Charing Cross and Westminster Medical School, London, United Kingdom.
3 To whom requests for reprints should be addressed.
Received 10/28/94. Accepted 11/16/94.
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