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 …

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 …

Chronic myeloid leukemia (CML) is a clonal bone marrow stem cell neoplasia known to be
responsive to immunotherapy. Despite the success of tyrosine kinase inhibitors (TKIs) …

The leukemic stem cells in patients with chronic myeloid leukemia (CML) are well known to
be clinically resistant to conventional chemotherapy and may also be relatively resistant to …

Chronic myeloid leukaemia (CML) is a clonal myeloproliferative disorder characterized by
the presence of a fusion oncogene BCR‐ABL, which encodes a protein with constitutive TK …

Imatinib therapy, which targets the oncogene product BCR-ABL, has transformed chronic
myeloid leukemia (CML) from a life-threatening disease into a chronic condition. Most …

The introduction of the BCR–ABL kinase inhibitor imatinib mesylate (Gleevec; Novartis)
revolutionized the treatment of chronic myeloid leukaemia (CML). However, most patients …

The BCR-ABL oncoprotein of chronic myelogenous leukemia (CML) localizes to the cell
cytoplasm, where it activates proliferative and antiapoptotic signaling pathways. We …

Chronic myeloid leukemia (CML) is caused by the Philadelphia (Ph+) chromosome carrying
the BCR-ABL oncogene, a constitutively active tyrosine kinase. The discovery of imatinib …

Bcr-Abl is the major cause and pathogenetic principle of chronic myeloid leukemia (CML).
Bcr-Abl results from a chromosomal translocation that fuses the bcr and abl genes, thereby …