Myeloproliferative disorders (MPD) are stem cell–derived clonal diseases arising as a
consequence of acquired aberrations in c-ABL, Janus-activated kinase 2 (JAK2), and …

Intracellular oxidative stress in cells transformed by the BCR-ABL oncogene is associated
with increased DNA double-strand breaks. Imprecise repair of these breaks can result in the …

Genomic instability is a hallmark of chronic myeloid leukemia in chronic phase (CML-CP)
resulting in BCR-ABL1 mutations encoding resistance to tyrosine kinase inhibitors (TKIs) …

Resistance to imatinib (IM) and other tyrosine kinase inhibitors (TKI) s is an increasing
problem in leukemias caused by expression of BCR-ABL1. As chronic myeloid leukemia …

Genes encoding c-ABL kinase and BCR protein are targeted by yet-unknown mechanisms
causing DNA double-strand breaks resulting in the generation of a chimeric gene encoding …

BCR/ABL-transformed chronic myeloid leukemia (CML) cells accumulate numerous DNA
double-strand breaks (DSB) induced by reactive oxygen species (ROS) and genotoxic …

Imatinib inhibits the kinase activity of Bcr-Abl and is currently the most effective drug for
treatment of chronic myeloid leukemia (CML). Imatinib also blocks c-Abl, a physiological …

BCR/ABL kinase–positive chronic myelogenous leukemia (CML) cells display genomic
instability leading to point mutations in various genes including bcr/abl and p53, eventually …

Mutations in the BCR/ABL kinase domain play a major role in resistance to imatinib
mesylate (IM). We report here that BCR/ABL kinase stimulates reactive oxygen species …

Chronic myeloid leukemia (CML) is induced by BCR-ABL1 and can be effectively treated for
many years with Imatinib until leukemia cells acquire drug resistance through BCR-ABL1 …