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Breakthrough in the treatment of chronic myeloid leukemia
https://aino.repo.nii.ac.jp/records/375
https://aino.repo.nii.ac.jp/records/375eb1c09a5-75c8-4c82-9c0c-cd7bccfe176b
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
KJ00008182379.pdf (411.0 kB)
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| 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 | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | CML | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | Philadelphia chromosome | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | BCR-ABL | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | tyrosine kinase | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | 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 | |||||
| 雑誌書誌ID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA11877461 | |||||
| ページ属性 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | P | |||||
| 論文名よみ | ||||||
| タイトル | Breakthrough in the treatment of chronic myeloid leukemia | |||||
| 著者 |
YAMADA, Yoshihiro
× YAMADA, Yoshihiro |
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| 著者所属(英) | ||||||
| 言語 | en | |||||
| 値 | Department of Physical Therapy,Faculty of Nursing and Rehabiitation,Aino University | |||||
| 記事種別(英) | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | Review article | |||||
| 抄録(英) | ||||||
| 内容記述タイプ | Other | |||||
| 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. | |||||
| 書誌情報 |
en : Aino journal 巻 10, 発行日 2012-03-31 |
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| 表示順 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 5 | |||||
| アクセション番号 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | KJ00008182379 | |||||
| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 1348480X | |||||
