By Toshihisa Ishikawa, John Schuetz
ABC Transporters and Cancer presents important info at the intriguing and fast-moving box of melanoma study. the following, remarkable and unique reports are provided on a number of issues. This quantity covers ABC transporters and melanoma, and is appropriate for researchers and scholars alike.
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ABC Transporters and melanoma offers worthwhile details at the fascinating and fast-moving box of melanoma study. right here, striking and unique studies are awarded on a number of issues. This quantity covers ABC transporters and melanoma, and is acceptable for researchers and scholars alike. presents info on melanoma researchOutstanding and unique reviewsSuitable for researchers and scholars
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Extra resources for ABC Transporters and Cancer
In the clinic, several studies have assessed polymorphisms in the genes encoding ABC transporters and tried to correlate these with drug pharmacokinetics and sometimes with the outcomes of anticancer drug treatments. These studies are very useful to understand the clinical use of ABC transporters as predictive markers for therapy response (Erdem, Giovannetti, Leon, Honeywell, & Peters, 2012; Pander, Guchelaar, & Gelderblom, 2010; Tang, Hendrikx, Beijnen, & Schinkel, 2013); however, assessment of the role of these transporters in anticancer disposition in patients remains challenging.
Obviously, also the level of expression of the tested ABC transporters and background expression of other transporters in the cell systems used is critical for assay sensitivity. ATP-dependent vesicular accumulation assays using inside-out vesicles can also be sensitive, but for hydrophobic drug substrates high aspecific background binding is often a problem. Other assays such as in vitro ATPase stimulation by tested drugs of ABC drug efflux proteins, or studying inhibition by such drugs of ABC protein activity in various assays, can be highly informative on the interaction of the drugs with the transporters but do not necessarily correlate with the overall efficacy of transmembrane transport.
This indicates that oral uptake of crizotinib was restricted only by Abcb1a/1b and that this Abcb1a/1b activity was saturable. In vitro, crizotinib was an ABCB1 but not an Abcg2 substrate. , 2011). This means that oral uptake of axitinib at the used dose (10 mg/kg) is restricted by Abcg2, but not by Abcb1a/1b. , 2012). , 2012). Yang et al. (2010) showed that oral availability of tandutinib was also increased in both the single and the combination knockout mice of Abcb1a/1b and Abcg2 compared to WT mice, indicating that both of these transporters limit the oral uptake of this drug.