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- W2014733477 abstract "Clinical resistance to imatinib often occurs in the absence of a mutation in the BCR-ABL kinase domain. Imatinib is transported out of cells by the efflux transporter ABCB1 (MDR1, whose product is p-glycoprotein). By contrast, the influx transporter, human organic cation transporter 1 (hOCT1) (also known as SLC22A1), transports imatinib into cells. Recent studies have identified that patients with low expression or activity of hOCT1 have a lower probability of achieving a cytogenetic or molecular remission. Prospective studies are currently investigating whether early trends in transporter expression can be used to guide treatment decisions. Plasma imatinib levels are higher in patients responding well to treatment, and may be useful in patients with suboptimal response or dubious compliance. Uptake of the second generation tyrosine kinase inhibitors, dasatinib and nilotinib, is less dependent upon hOCT1. These two drugs may therefore achieve adequate intracellular concentrations even in patients with low hOCT1 expression." @default.
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- W2014733477 date "2008-01-01" @default.
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- W2014733477 title "Pharmacologic markers and predictors of responses to imatinib therapy in patients with chronic myeloid leukemia" @default.
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- W2014733477 doi "https://doi.org/10.1080/10428190701858823" @default.
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