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Imatinib mesylate, a Bcr-Abl kinase inhibitor, has been very successful in
the treatment of chronic myelogenous leukemia (CML). However, the majority of
patients achieving cytogenetic remissions with imatinib treatment have molecular
evidence of persistent disease, and residual BCR/ABL(+) progenitors can be
detected. There is a need to develop new approaches that enhance elimination of
malignant progenitors in imatinib-treated patients.
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