Abstract
Clinical significance of T315I ABL kinase domain mutation detection in patients resistant to imatinib mesylate therapy
Highlights
Chronic myeloid leukemia (CML) is a myeloproliferative disease characterized by chromosomal translocation t(9;22) (q34;q11), known as Philadelphia chromosome
T315I detection is essential in therapy approach for CML patients as the treatment of choice for T315I carriers is stem-cell transplantation
Izoleucin sadrži jednu ugljikovodikovu skupinu više u postraničnom lancu, koja stvara steričke smetnje za vezivanje tyrosine kinase inhibitor (TKI), ali ne Chronic myeloid leukemia (CML) is a myeloproliferative disease characterized by chromosomal translocation t(9;22) (q34;q11), known as Philadelphia chromosome
Summary
Chronic myeloid leukemia (CML) is a myeloproliferative disease characterized by chromosomal translocation t(9;22) (q34;q11), known as Philadelphia chromosome. The consequence of this translocation is a bcr-abl oncogenic fusion gene which produces bcr-abl protein with enhanced tyrosine kinase activity. Chronic myeloid leukemia (CML) is a myeloproliferative disease characterized by the presence of bcr-abl fusion gene and bcr-abl fusion protein. The discovery of tyrosine kinase inhibitor (TKI), imatinib mesylate (IM), improved the treatment of CML patients, a proportion of patients develop resistance to the drug resulting in increased bcr-abl level. The aim of this study was to detect if the presence of T315I in patients resistant to imatinib mesylate therapy is associated with the increase or constantly high bcr-abl level. We aimed to assess the possible di erence in bcr-abl level in imatinib-resistant patients with and without T315I mutation
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