Abstract
There are several lines of evidences reactive oxygen species (ROS) appear to play a major role in leukemogensis. BCR/ABL oncogenic tyrosine kinase is known to induce high levels of intracellular ROS which may further induce genomic instability with malignant transformation and even imatinib (IM) resistance. Disrupting of intracellular ROS levels and redox signaling could inhibit tumor cell growth. In this study, we investigated the changes of peroxiredoxin (PRX) and ROS levels during IM therapy in BCR-ABL positive leukemia cells.
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