Comprehensive UGT1A1 Genotyping in a Japanese Pop-
نویسندگان
چکیده
ulation by Pyrosequencing, Mayumi Saeki, Yoshiro Saito, Hideto Jinno, Masahiro Tohkin, Kouichi Kurose, Nahoko Kaniwa, Kazuo Komamura, Kazuyuki Ueno, Shiro Kamakura, Masafumi Kitakaze, Shogo Ozawa, and Jun-ichi Sawada ( Project Team for Pharmacogenetics, 2 Division of Biochemistry and Immunochemistry, 3 Division of Environmental Chemistry, 4 Division of Medicinal Safety Science, and 8 Division of Pharmacology, National Institute of Health Sciences, 1-18-1, Kamiyoga, Setagayaku, Tokyo 158-8501, Japan; 5 Division of Cardiology, 6 Department of Cardiovascular Dynamics Research Institute, and 7 Department of Pharmacy, National Cardiovascular Center, 5-7-1, Fujishirodai, Suita, Osaka 565-8565, Japan; * address correspondence to this author at: Division of Biochemistry and Immunochemistry, National Institute of Health Sciences, 1-18-1, Kamiyoga, Setagaya-ku, Tokyo 158-8501, Japan; fax 81-3-3707-6950, e-mail yoshiro@nihs. go.jp)
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Influence of UGT1A1 6, 27, and 28 polymorphisms on nilotinib-induced hyperbilirubinemia in Japanese patients with chronic myeloid leukemia.
Nilotinib potently inhibits human uridine diphosphate-glucuronosyltransferase (UGT1A1) activity, causing hyperbilirubinemia. We investigated the influence of UGT1A1 polymorphisms and nilotinib plasma trough concentrations (C0) on nilotinib-induced hyperbilirubinemia in 34 Japanese patients with chronic myeloid leukemia (CML). The proportion of patients with hyperbilirubinemia was significantly ...
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