Chronic myeloid leukemia (CML) is driven by the constitutive activity of the BCR-ABL1 fusion
oncoprotein. Despite the great success of drugs that target the BCR-ABL1 ATP-binding site …

Because imatinib (IM) resistance in chronic myeloid leukemia is primarily caused by the re‐
establishment of Abl kinase, new inhibitors may be efficacious. We evaluated 3 new agents …

The most common mechanism of relapse for CML patients treated with Imatinib is the
appearance of point mutations in the BCR-ABL oncogene that confer resistance to this drug …

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 of the ABL kinase domain (KD) are common in patients with chronic myelogenous
leukemia (CML) who develop resistance to imatinib. We developed an RT-PCR-based …

Treatment of chronic myeloid leukemia (CML) has changed drastically with the emergence
of the Abl tyrosine kinase inhibitor (TKI), imatinib mesylate. However, primary and secondary …

Chronic myeloid leukemia (CML) was the first human malignant disease to be linked to a
single, acquired genetic abnormality. Identification of the BCR-ABL kinase fusion protein …

The emergence of resistance to imatinib (IM) mediated by mutations in the BCR-ABL domain
has become a major challenge in the treatment of chronic myeloid leukemia (CML). Here …

A new SRC-Abl dual inhibitor, BMS354825, has recently been presented as a possible tool
to overcome resistance to imatinib in neoplasias caused by oncogenic variants of the …

6519 Background: Resistance to imatinib in CML patients is often associated with Bcr-Abl
point mutations which interfere with imatinib binding. BMS-354825 is a novel, orally …