In advanced-phase chronic myeloid leukemia (CML), resistance to imatinib mesylate is
associated with point mutations in the BCR-ABL kinase domain. A new generation of potent …

Patients with advanced stages of chronic myeloid leukemia (CML) often manifest imatinib
mesylate resistance associated with point mutations in BCR-ABL. AMN107 is a new higher …

Drug resistance resulting from emergence of imatinib-resistant BCR-ABL point mutations is
a significant problem in advanced-stage chronic myelogenous leukemia (CML). The BCR …

Targeted therapy with the Abl kinase inhibitor imatinib has markedly improved the outlook
for patients with chronic myeloid leukemia (CML). Breakpoint cluster region (Bcr)-Abl …

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 …

Chronic myeloid leukemia is effectively treated with imatinib, but reactivation of BCR-ABL
frequently occurs through acquisition of kinase domain mutations. The additional approved …

Data demonstrating the superiority of nilotinib over imatinib in the frontline treatment of
chronic myeloid leukemia (CML) and ongoing studies with dasatinib and bosutinib are …

Despite the efficacy of imatinib therapy in chronic myelogenous leukemia, the development
of resistance continues to challenge the treatment of this disease. Mutations within the …

BCR-ABL1 compound mutations can confer high-level resistance to imatinib and other ABL1
tyrosine kinase inhibitors (TKIs). The third-generation ABL1 TKI ponatinib is effective against …

Nilotinib, an orally bioavailable, selective Bcr-Abl tyrosine kinase inhibitor, is 30-fold more
potent than imatinib in pre-clinical models, and overcomes most imatinib resistant BCR-ABL …