Abstract
The Philadelphia (Ph) chromosome breakpoints in chronic myelocytic leukaemia are clustered on chromosome 22 band qll in a 5.8-kilobase (kb) region designated bcr1. The c-abl protooncogene is translocated from chromosome 9 band q34 into bcr and the biochemical consequence of this molecular rearrangement is the production of an abnormal fusion proteinbcr–abl p210 with enhanced protein-tyrosine kinase activity2,3 compared to the normal p145 c-abl protein. The Ph chromosome translocation is also seen in some acute lymphoblastic leukaemias with B-cell precursor phenotypes4,5 some of which have bcr rearrangement (bcr+) and some do not (bcr-)6,7. We present evidence that the Ph+, bcr- leukaemias are associated with a novel p190 abl kinase. We propose that acute lymphoblastic leukaemias that are bcr+, p210+ are probably lymphoid blast crises following a clinically silent chronic phase of chronic myelocytic leukaemia arising in multipotential stem cells whereas bcr- p190+ cases are de novo acute lymphoblastic leukaemias arising in more restricted precursors.
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Chan, L., Karhi, K., Rayter, S. et al. A novel abl protein expressed in Philadelphia chromosome positive acute lymphoblastic leukaemia positive acute lymphoblastic leukaemia. Nature 325, 635–637 (1987). https://doi.org/10.1038/325635a0
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DOI: https://doi.org/10.1038/325635a0
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