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Selective inhibition of the BCR/ABL tyrosine kinase by imatinib has become
a first-line therapy for chronic myelogenous leukemia (CML). However,
BCR/ABL-positive progenitors often persist despite treatment, and relapse
associated with resistance to imatinib has been described in many patients with
advanced disease. Drug efflux by P-glycoprotein (P-gp), as well as point
mutations in BCR/ABL oncoprotein, has been implicated in the mechanism of
resistance to imatinib. In this study, we established a murine transplantation
model of CML-like myeloproliferative disease using Mdr1a/1b-null mice and
analyzed the effects of loss of P-gp on resistance to imatinib.
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