@article{oai:kumadai.repo.nii.ac.jp:00024853,
 author = {山川, 裕司 and 濱田, 哲暢 and 首藤, 剛 and 結城, 美里 and 内田, 隆 and 甲斐, 広文 and 川口, 辰哉 and 齋藤, 秀之 and Yamakawa, Yuji and 濱田, 哲暢 and Hamada, Akinobu and Shuto, Tsuyoshi and Yuki, Misato and Uchida, Takashi and Kai, Hirofumi and Kawaguchi, Tatsuya and Saito, Hideyuki},
 issue = {1},
 journal = {Clinical Pharmacology and Therapeutics},
 month = {Jul},
 note = {application/pdf, 論文(Article), The purpose of this study was to explore the role of the organic-anion transporting polypeptide (OATP) 1A2 that is encoded by SLCO1A2, in the cellular uptake of the BCR-ABL tyrosine kinase inhibitor imatinib, and the relationship between SLCO1A2 polymorphisms and the pharmacokinetics of imatinib in chronic myeloid leukemia (CML) patients. Imatinib uptake was significantly enhanced in OATP1A2-transfected human embryonic kidney (HEK)293 cells (P=0.002). Naringin, an OATP1A2 inhibitor, decreased the transport of imatinib in OATP1A2-transfected HEK293, the human intestinal cell line Caco-2, and the CML cell line K562 cells. Linkage disequilibrium was found between the SLCO1A2 -1105G>A and -1032G>A genotypes in 34 CML patients and 100 healthy subjects. Imatinib clearance of CML patients was influenced by the SLCO1A2 -1105G>A/-1032G>A genotype (P=0.075) and the SLCO1A2 -361GG genotype (P=0.005). These findings suggest that imatinib is transported into cells by OATP1A2, and that SLCO1A2 polymorphisms significantly affect imatinib pharmacokinetics., http://www.nature.com/clpt/journal/v90/n1/full/clpt2011102a.html},
 pages = {157--163},
 title = {Pharmacokinetic impact of SLCO1A2 polymorphisms on imatinib disposition in patients with chronic myeloid leukemia},
 volume = {90},
 year = {2011},
 yomi = {ハマダ, アキノブ}
}