Imatinib (mesylate)

Detection of BCR-ABL Mutations and Resistance to Imatinib Mesylate

The major mechanism of imatinib resistance for patients with chronic myeloid leukemia (CML) is clonal expansion of leukemic cells with mutations in the Bcr-Abl fusion tyrosine kinase that reduce the capacity of imatinib to inhibit kinase

Detection of BCR-ABL1 Kinase Domain Mutations Causing Imatinib Resistance in Chronic Myelogenous Leukemia

and quantitate the tumor-specific BCR-ABL1 RNA have been shown to be an ultrasensitive diagnostic, prognostic, and monitoring tool for Philadelphia-positive leukemias. A novel tyrosine kinase inhibitor (TKI), imatinib, has been confirmed as an effective targeted

Therapeutic Targeting of Gene Expression by siRNAs Directed Against BCR-ABL Transcripts in a Patient with Imatinib-Resistant Chronic Myeloid Leukemia

RNAi. Here we show that in vivo application of targeted nonvirally delivered synthetic bcr-abl siRNA in a female patient with recurrent Philadelphia chromosome positive chronic myeloid leukemia (CML) resistant to imatinib (Y253F mutation