Similar molecular alterations occur in related leukemias with and without the Philadelphia chromosome.

The reciprocal translocation between the long arms of chromosomes 9 and 22, t(9 : 22), results in the Philadelphia (Ph1) chromosome, the karyotypic hallmark of chronic myeloid leukaemia (CML) [1]. The molecular consequences of this translocation have been well characterized, although their contribution to the disease process is less clear. The translocation creates a hybrid transcription unit consisting of the 5' end of the so-called breakpoint cluster region (ber) gene on ch22q 11 and the e-abl proto-oncogene on ch9q34 [2]. This new gene is capable of being expressed as a chimeric 8.7 kb mRNA [3] which, when translated, produces a fusion protein (p210) with an enhanced phosphorylating activity [4] compared, in vitro, to the normal e-abl protein (p145). This translocation event can be seen at the DNA level in the ber gene, since it usually occurs within an 5.8 kb region of DNA and can be detected with a specific probe for this region (bcr probe) [2]. Involvement of e-abl is more difficult to demonstrate since the break on ch9q34 can occur anywhere within 50 kb or more [5] upstream of the proto-oncogene. We therefore chose to look at the size of the abl protein-tyrosine kinase as well as the level of its activity, as an assay for eabl involvement. Using these criteria we analysed two other types of leukaemias (a) Ph1-positive acute lymphoblastic leu-