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  1. AINO JOURNAL
  2. vol.10(2012.3.31)

Breakthrough in the treatment of chronic myeloid leukemia

https://aino.repo.nii.ac.jp/records/375
https://aino.repo.nii.ac.jp/records/375
eb1c09a5-75c8-4c82-9c0c-cd7bccfe176b
名前 / ファイル ライセンス アクション
KJ00008182379.pdf KJ00008182379.pdf (411.0 kB)
Item type [ELS]紀要論文 / Departmental Bulletin Paper(1)
公開日 2019-03-27
タイトル
タイトル Breakthrough in the treatment of chronic myeloid leukemia
言語 en
言語
言語 eng
キーワード
主題 CML, Philadelphia chromosome, BCR-ABL, tyrosine kinase, imatinib
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ departmental bulletin paper
著者 Yamada, Yoshihiro

× Yamada, Yoshihiro

en Yamada, Yoshihiro

ja ISNI

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抄録(英)
内容記述タイプ Abstract
内容記述 Chronic myeloid leukemia (CML) was once a life-threatening disease in which the clonal expansion of leukemic myeloid cells occurs as a result of reciprocal chromosomal translocation between long arm of chromosome 9 and 22 (Philadelphia chromosome). The resulting fusion protein BCR-ABL shows constantly activated ABL tyrosine kinase activity which is essential for growth of leukemic cells. Specific inhibition of this activated tyrosine kinase by imatinib (Gleevec, Novartis) has completely changed the curability of the disease (Druker et al., 2001). Imatinib is designed to inhibit the binding of ATP to the ABL tyrosine kinase so as to abolish the phosphorylation of the downstream signal proteins. Chronic myeloid leukemia is one of the diseases of which the molecular mechanism of development has been best dissected. And the discovery of imatinib is truly a milestone and the victory for modern molecular medicine. Its amazing efficacy has transformed a disease with a formidable prognosis, CML, into a chronic condition with safety well established. Imatinib now being a standard therapy for CML, the history of the study of the molecular mechanism of CML, the discovery of the drug, and the related questions are discussed.
言語 en
書誌情報 en : Aino journal

巻 10, 号 1, p. 17-21, ページ数 5, 発行日 2012-03-31
ISSN
収録物識別子タイプ PISSN
収録物識別子 1348480X
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