Docking simulations were used to predict the most favorable interaction between the T315I
mutated form of Abl (invariably associated with resistance to the tyrosine kinase inhibitor …

Abstract The Bcr-Abl tyrosine kinase (TK) is the molecular hallmark of chronic myeloid
leukemia (CML). Src is another TK kinase whose involvement in CML was widely …

Monotherapy of chronic myeloid leukemia (CML) with imatinib mesylate has been cast into
shadow by the evolution of clinical resistance during therapy. Resistance to imatinib can …

Mutation in the ABL kinase domain is the principal mechanism of imatinib resistance in
patients with chronic myelogenous leukemia. Many mutations favor active kinase …

Acquired resistance to the ABL tyrosine kinase inhibitor (TKI) imatinib is a significant clinical
problem for patients with chronic myeloid leukemia (CML), where a major resistance …

A family of dual Src/Abl inhibitors characterized by a substituted pyrazolo [3, 4-d] pyrimidine
scaffold was previously reported by us and proved to be active against several tumor cell …

The tyrosine kinase Src and its close homolog Abl, both play important roles in chronic
myelogenous leukemia (CML) progression and Imatinib resistance. No clinically approved …

Large-scale (∼ 36,000 atoms) long-time (30 ns each) molecular dynamics (MD) simulations
on the complex of imatinib and 16 common mutants of the ABL tyrosine kinase domain have …

Structural studies suggest that most point mutations in the BCR-ABL kinase domain cause
resistance to the ABL kinase inhibitor imatinib by impairing the flexibility of the kinase …

Chronic myeloid leukemia (CML) was the first neoplastic disease for which the knowledge of
the molecular pathogenesis led to the development of a curative therapy. Imatinib mesylate …