• Leukemia research · Dec 2003

    Case Reports

    ABL-kinase domain point mutation as a cause of imatinib (STI571) resistance in CML patient who progress to myeloid blast crisis.

    • Tomasz Sacha, Andreas Hochhaus, Benjamin Hanfstein, Martin C Müller, Zbigniew Rudzki, Jacek Czopek, Teresa Wolska-Smoleń, Sylwia Czekalska, Zoriana Salamanchuk, Malgorzata Jakóbczyk, and Aleksander B Skotnicki.
    • Department of Haematology, Jagiellonian University Medical College, Cracow, Poland. mmsacha@cyf-kr.edu.pl
    • Leuk. Res. 2003 Dec 1; 27 (12): 1163-6.

    AbstractImatinib mesylate (STI571) is a major therapeutic advance for the management of chronic myeloid leukaemia (CML), however, a proportion of patients are refractory to it, particularly those in more advanced phases of CML. Different mechanisms of resistance to imatinib are suggested, including point mutations within ABL-kinase domains. A point mutation leading to substitution at the ATP binding site of ABL-kinase and insensitivity to imatinib was detected in our patient treated with imatinib, who progressed to blast crisis. Additionally, clonal evolution could lead to BCR-ABL-independent proliferation. Early detection of ABL-kinase mutation could predict the progression of CML treated with imatinib.

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