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) …

Chronic myelogenous leukemia (CML) arises from the constitutive activity of the BCR-ABL1
oncoprotein. Tyrosine kinase inhibitors (TKIs) that target the ATP-binding site have …

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 …

Point mutations were found in the adenosine triphosphate (ATP) binding region of BCR/ABL
in 12 of 18 patients with chronic myeloid leukemia (CML) or Ph-positive acute lymphoblastic …

Background Although the vast majority of patients with chronic myeloid leukemia (CML)
respond to the tyrosine kinase inhibitor (TKI) imatinib mesylate, resistance might occur de …

Background: Asciminib is a potent and specific BCR‐ABL1 inhibitor that binds to the
myristoyl pocket of ABL1. Preclinical data suggest cooperativity when asciminib is combined …

Chronic myeloid leukemia cells acquire resistance to tyrosine kinase inhibitors through
mutations in the ABL1 kinase domain. The T315I mutation mediates resistance to imatinib …

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 …

Acquired resistance through genetic mutations is a common phenomenon in several cancer
therapies using molecularly targeted drugs, best exemplified by the BCR-ABL inhibitor …

The introduction of the tyrosine kinase inhibitors (TKIs) imatinib, dasatinib, and nilotinib has
dramatically improved the treatment of chronic myeloid leukemia (CML). However, a minority …