Abstract Increased levels of Bcr-Abl expression in chronic myelogenous leukemia (CML)
cells are associated with disease progression and imatinib (IM) resistance. However, it is not …

BCR-ABL overexpression and stem cell quiescence supposedly contribute to the failure of
imatinib mesylate (IM) to eradicate chronic myeloid leukemia (CML). However, BCR-ABL …

Abstract Mutations in the Bcr-Abl kinase domain are a frequent cause of imatinib resistance
in patients with advanced CML or Ph+ ALL. The impact of these mutations on the overall …

A characteristic feature of chronic myeloid leukaemia (CML) is the inevitable advancement
from a treatable chronic phase to a fatal, drug-resistant stage referred to as blast crisis. The …

The BCR-ABL oncogenic tyrosine kinase causes chronic myeloid leukemia and is the target
for imatinib therapy. During imatinib treatment, cells are selected in some patients with BCR …

Retroviral transduction of the BCR-ABL kinase into primary mouse bone marrow cells
lacking the Arf tumor suppressor rapidly generates polyclonal populations of continuously …

As chronic myeloid leukemia (CML) progresses from the chronic phase to blast crisis, the
levels of BCR-ABL increase. In addition, blast-transformed leukemic cells display enhanced …

Imatinib mesylate (IM) binds to the BCR-ABL protein, inhibiting its kinase activity and
effectively controlling diseases driven by this kinase. IM resistance has been associated with …

The BCR-ABL kinase inhibitor imatinib mesylate induces complete cytogenetic response
(CCR) in a high proportion of chronic myelogenous leukemia (CML) patients. However …

Imatinib mesylate (Gleevect, formerly STI571) is a specific small molecule inhibitor that
targets the Bcr-Abl tyrosine kinase, the causative oncogene of chronic myelogenous …