Abstract：
:Chronic myeloid leukemia shown to be associated with the Ph translocation,--characterised as a t(9;22)--, joins the bcr and abl genes and leads to expression of chimeric BCR-ABL protein with enhanced tyrosine kinase (TK) activity. This increased TK activity leads to malignant transformation by interference with the control of proliferation, cellular adherence and apoptosis. The presence of this protein in every CML cells is strong evidence of its pathogenetic role. Following this observations efforts were made to develop molecularly targeted therapies for CML. The specific inhibitor of BCR-ABL TK, STI571 was developed by Brian Druker and his co-workers in 1996. STI571 (Signal Transduction Inhibitor) occupies the kinase pocket of the BCR-ABL protein, and blocks ATP binding, thereby preventing phosphorylation of any substrate. Because of promising preclinical data STI571 entered clinical trials in 1998, using an oral formulation. The reports of this trials document excellent efficacy. Patients with chronic phase after failure with interferon therapy achieved more than 90% hematologic response, usually within 4-6 weeks, and 55% major cytogenetic response. Patients with advanced disease also responded, though less durably. In phase 2 studies the drug has continued to produce impressive results. STI571 has a very favourable pharmacologic feature, with high degree of specificity for its target, and therefore low toxicity for normal tissues, it is well tolerable, side effects were minimal. STI571 opens a new era in the treatment of malignancies, it is the first targeted molecular therapy which is able to target abnormal cells without damaging normal cells, compared with traditional antineoplastic drugs.
journal_name
Orv Hetiljournal_title
Orvosi hetilapauthors
Molnár L,Losonczy Hsubject
Has Abstractpub_date
2002-10-20 00:00:00pages
2379-84issue
42eissn
0030-6002issn
1788-6120journal_volume
143pub_type
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