Rapid Sequential Gain of ABL1 Kinase Domain Mutations with a Complex Karyotype in the Progression of Chronic Myelogenous Leukemia
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CML is a myeloproliferative disease characterized by the Phila- delphia (Ph) chromosome, in which the oncogenic BCR-ABL1 fusion gene encodes a constitutively active tyrosine kinase. First- line treatment using the BCR-ABL tyrosine kinase inhibitor (TKI) imatinib has significantly changed the disease course of CML [1]. However, some patients develop resistance to this agent, largely due to point mutations within the ABL1 kinase domain (KD) [2, 3]. Resistance to imatinib may be overcome by treatment with second-line TKIs, including dasatinib, nilotinib, and bosutinib, which are active against most mutations; however, some muta- tions bring about resistance to these second-line drugs as well [4-6]. Therefore, a mutation analysis is recommended when choosing a second-line TKI [7]. We describe a CML patient who rapidly progressed to blast crisis following the sequential acquisi- tion of ABL1 KD mutations with a complex karyotype.
Abstract
CML is a myeloproliferative disease characterized by the Phila- delphia (Ph) chromosome, in which the oncogenic BCR-ABL1 fusion gene encodes a constitutively active tyrosine kinase. First- line treatment using the BCR-ABL tyrosine kinase inhibitor (TKI) imatinib has significantly changed the disease course of CML [1]. However, some patients develop resistance to this agent, largely due to point mutations within the ABL1 kinase domain (KD) [2, 3]. Resistance to imatinib may be overcome by treatment with second-line TKIs, including dasatinib, nilotinib, and bosutinib, which are active against most mutations; however, some muta- tions bring about resistance to these second-line drugs as well [4-6]. Therefore, a mutation analysis is recommended when choosing a second-line TKI [7]. We describe a CML patient who rapidly progressed to blast crisis following the sequential acquisi- tion of ABL1 KD mutations with a complex karyotype.
참고문헌 (14)
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