Molecularly targeted kinase inhibitor cancer therapies are currently administered
sequentially rather than simultaneously. We addressed the potential long-term impact of this …

Chronic myeloid leukemia (CML), caused by constitutively active BCR-ABL1 fusion tyrosine
kinase, has served as a paradigm for successful application of molecularly targeted cancer …

Mutations in the kinase domain (KD) of BCR-ABL are the most prevalent mechanism of
acquired imatinib resistance in patients with chronic myeloid leukemia (CML). Here we …

Imatinib, a small-molecule ABL kinase inhibitor, is a highly effective therapy for early-phase
chronic myeloid leukaemia (CML), which has constitutively active ABL kinase activity owing …

Purpose: Chronic myeloid leukemia (CML) is effectively treated with imatinib. However,
reactivation of Bcr-Abl via kinase domain mutations that reduce sensitivity to imatinib can …

The acquisition of mutations within the BCR-ABL1 kinase domain is frequently associated
with tyrosine kinase inhibitor (TKI) failure in chronic myeloid leukemia. Sensitive sequencing …

Purpose Point mutations within the ABL kinase domain of the BCR-ABL gene have been
associated with clinical resistance to imatinib mesylate in chronic myeloid leukemia (CML) …

Purpose BCR-ABL1 mutation analysis is recommended to facilitate selection of appropriate
therapy for patients with chronic myeloid leukemia after treatment with imatinib has failed …

Every year, more than 8000 new cases of chronic myeloid leukemia (CML) are diagnosed in
the United States. 1 BCR-ABL1, a fusion protein kinase derived from a reciprocal …

Inhibition of BCR-ABL by imatinib induces durable responses in many patients with chronic
myeloid leukemia (CML), but resistance attributable to kinase domain mutations can lead to …