Chronic myeloid leukemia is still the most characteristic entity of the chronic myeloproliferative diseases. The tumor promoter role of abl-dependent tyrosine kinase activation, which is enhanced by bcr/abl rearrangement (due the classical translocation of Philadelphia chromosomal abnormality) has been quite well clarified. The better understanding of the role of altered cell signalling pathways in the pathogenesis of chronic myeloid leukaemia opened new areas for extensive and fruitful pharmacological research. The first, non-myelosuppressive agent, which was able to reduce the number of Philadelphia positive clonal cells was the interferon group, which drug could substantially prolong the chronic phase and mortality of chronic myeloid leukaemia. Imatinib mesylate, a tyrosine-kinase inhibitor seemes to able to produce clinical and major cytogenetic response in more than 80% of patients. Imatinib is also a powerful agent in the accelerated or blastic phased of chronic myeloid leukaemia. With the advent of these new drugs the therapeutic algorhythm of chronic myeloid leukaemia and allogeneous bone marrow transplantation seems to be reconsidered, too.
|Translated title of the contribution||Chronic myeloid leukemia|
|Number of pages||5|
|Publication status||Published - Dec 1 2005|
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