Combination with a defucosylated anti-HM1.24 monoclonal antibody plus lenalidomide induces marked ADCC against myeloma cells and their progenitors

• 資料種別: 博士論文
• タイトル: Combination with a defucosylated anti-HM1.24 monoclonal antibody plus lenalidomide induces marked ADCC against myeloma cells and their progenitors
• 著者・編者: Harada, Takeshi; Ozaki, Shuji; Oda, Asuka; Tsuji, Daisuke; Ikegame, Akishige; Iwasa, Masami; Udaka, Kengo; Fujii, Shiro; Nakamura, Shingen; Miki, Hirokazu; Kagawa, Kumiko; Kuroda, Yoshiaki; Kawai, Shigeto; Itoh, Kohji; Yamada-Okabe, Hisafumi; Matsumoto, Toshio; Abe, Masahiro
• 著者標目: Harada, Takeshi; Ozaki, Shuji; Oda, Asuka; Tsuji, Daisuke; Ikegame, Akishige; Iwasa, Masami; Udaka, Kengo; Fujii, Shiro; Nakamura, Shingen; Miki, Hirokazu; Kagawa, Kumiko; Kuroda, Yoshiaki; Kawai, Shigeto; Itoh, Kohji; Yamada-Okabe, Hisafumi; Matsumoto, Toshio; Abe, Masahiro
• 出版事項: PLOS
• 出版年月日等: 2013-12-26
• 出版年（W3CDTF）: 2013-12-26
• 並列タイトル等: 低フコース化抗HM1.24抗体とレナリドミドの併用は骨髄腫細胞および骨髄腫細胞幹細胞に著明なADCC活性を示す; Combination of Defucosylated AHM plus Lenalidomide
• タイトル（掲載誌）: PLOS ONE
• 巻号年月日等（掲載誌）: 8 12
• 掲載巻: 8
• 掲載号: 12
• 掲載ページ: e83905-
• ISSN（掲載誌）: ISSN : 1932-6203
• 授与機関名: 徳島大学
• 授与年月日: 2014-03-24
• 報告番号: 甲第2668号
• 学位: 博士（医学）
• 本文の言語コード: eng
• 件名標目: Multiple myeloma; HM1.24; Lenalidomide; ADCC
• 対象利用者: 一般
• 一般注記: The immunomodulatory drug lenalidomide (Len) has drawn attention to potentiate antibody-dependent cellular cytotoxicity (ADCC)-mediated immunotherapies. We developed the defucosylated version (YB-AHM) of humanized monoclonal antibody against HM1.24 (CD317) overexpressed in multiple myeloma (MM) cells. In this study, we evaluated ADCC by YB-AHM and Len in combination against MM cells and their progenitors. YB-AHM was able to selectively kill via ADCC MM cells in bone marrow samples from patients with MM with low effector/target ratios, which was further enhanced by treatment with Len. Interestingly, Len also up-regulated HM1.24 expression on MM cells in an effector-dependent manner. HM1.24 was found to be highly expressed in a drug-resistant clonogenic ‘‘side population’’ in MM cells; and this combinatory treatment successfully reduced SP fractions in RPMI 8226 and KMS-11 cells in the presence of effector cells, and suppressed a clonogenic potential of MM cells in colony-forming assays. Collectively, the present study suggests that YB-AHM and Len in combination may become an effective therapeutic strategy in MM, warranting further study to target drug-resistant MM clonogenic cells.
• 記録形式（IMT）: application/pdf
• オンライン閲覧公開範囲: インターネット公開
• 著作権情報: Copyright: © 2013 Harada et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.( https://creativecommons.org/licenses/by/4.0/ )
• 関連情報（DOI）: 10.1371/journal.pone.0083905
• 連携機関・データベース: 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• 提供元機関・データベース: 徳島大学 : 徳島大学機関リポジトリ

目次

http://repo.lib.tokushima-u.ac.jp/files/public/10/106068/20170929144631600622/LID201404221012.pdf fulltext

http://repo.lib.tokushima-u.ac.jp/files/public/10/106068/20170929144631919137/LID201405281001.pdf fulltext