By Toshihisa Ishikawa, John Schuetz
ABC Transporters and Cancer presents helpful info at the intriguing and fast-moving box of melanoma study. right here, notable and unique experiences are offered on numerous themes. This quantity covers ABC transporters and melanoma, and is acceptable for researchers and scholars alike.
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Additional resources for ABC Transporters and Cancer
They are localized at the apical membranes of intestinal and renal proximal tubule epithelial cells and at the bile canalicular membranes of the hepatocytes, where they efflux their substrates into intestinal lumen or feces, urine, and bile to protect the organism (Fig. , 2009). They are also expressed at the apical membranes of blood–brain, blood–testis, and blood–placenta barriers, where they extrude endogenous or exogenous substrates, including drugs, carcinogens, and toxins, into the main circulation in order to protect those tissue sanctuaries (Fig.
3 Chemical inhibition of transporters to increase oral availability of rationally designed anticancer drugs In several preclinical studies, chemical inhibition of ABC transporters has been shown to improve oral availability of (rationally designed) anticancer drugs. , 2004). , 2012). Very likely the information gained from these preclinical studies can be used for translation to the clinical use of inhibitors to improve the oral bioavailability of chemotherapeutic agents. Several clinical investigations have been conducted for this reason, some of which, but not all, have been promising.
2012) demonstrated that the antitumor efficacy of orally coadministered paclitaxel and 20(S)-Ginsenoside Rg3, an ABCB1 inhibitor, against MCF-7 tumor xenografts in nude BALB/c mice was similar as intravenously administered paclitaxel at the same dose. , 2010). However, since plasma and tumor concentrations of paclitaxel were not measured during these tumor growth experiments, it remains unclear if inhibition of Abcb1a/1b took place primarily in intestinal and hepatic tissue or also in tumor tissue, and thus what was the primary cause of the improved antitumor efficacy: enhanced oral availability, or also increased tumor penetration of paclitaxel.