Abstract
Important advances in the understanding of the molecular basis of chronic myeloid leukemia have resulted in the development of new therapies and changed the paradigm for managing this myeloproliferative disease. The reciprocal translocation of the abl (Abelson murine leukemia) proto-oncogene on chromosome 9 to the bcr (breakpoint cluster region) gene on chromosome 22 creates a transcriptionally active, chimeric bcr-abl gene and gives rise to the Philadelphia chromosome. 1
 The genetic hallmark of chronic myeloid leukemia (CML) is the Philadelphia chromosome (Ph), which occurs in at least 95% of CML cases as well as some cases of acute lymphocytic leukemia (ALL; approximately 5% for children, 20% for adults). It also has been reported in some other hematologic disorders, albeit rarely. 2-4 JMS 2016; 19(2):95-96
Highlights
Important advances in the understanding of the molecular basis of chronic myeloid leukemia have resulted in the development of new therapies and changed the paradigm for managing this myeloproliferative disease
The genetic hallmark of chronic myeloid leukemia (CML) is the Philadelphia chromosome (Ph), which occurs in at least 95% of CML cases as well as some cases of acute lymphocytic leukemia (ALL; approximately 5% for children, 20% for adults)
The reciprocal translocation between chromosomes 9 and 22 places the 59 regulatory domains of the BCR gene from chromosome 22 in juxtaposition with the 39 tyrosine kinase domains of ABL from chromosome 9. This unique gene fusion leads to the expression of chimeric bcr-abl messenger RNA and the production of functional BCR-ABL fusion protein
Summary
Important advances in the understanding of the molecular basis of chronic myeloid leukemia have resulted in the development of new therapies and changed the paradigm for managing this myeloproliferative disease. The bcr-abl gene encodes a 190 or 210 kd protein product, which is an active, deregulated, intracellular tyrosine kinase.[1] By this mechanism, the fusion protein is thought to induce malignant transformation of hematopoietic stem cells.[5,6] The reciprocal translocation between chromosomes 9 and 22 places the 59 regulatory domains of the BCR gene from chromosome 22 in juxtaposition with the 39 tyrosine kinase domains of ABL from chromosome 9.
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