WEKO3
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Blockade of the ERK or PI3K-Akt signaling pathway enhances the cytotoxicity of histone deacetylase inhibitors in tumor cells resistant to gefitinib or imatinib.
http://hdl.handle.net/10069/22719
http://hdl.handle.net/10069/227190f29197f-fa0d-4c9d-8aa5-b2cfccaa1fec
名前 / ファイル | ライセンス | アクション |
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BBRC_Kohno.pdf (2.6 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2010-01-20 | |||||
タイトル | ||||||
タイトル | Blockade of the ERK or PI3K-Akt signaling pathway enhances the cytotoxicity of histone deacetylase inhibitors in tumor cells resistant to gefitinib or imatinib. | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Chronic myeloid leukemia | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Drug resistance | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | HDAC inhibitor | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | MEK inhibitor | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Non-small cell lung cancer | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | PI3K inhibitor | |||||
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 | journal article | |||||
著者 |
Ozaki, Kei-Ichi
× Ozaki, Kei-Ichi× Kosugi, Masaki× Baba, Nobuyuki× Fujio, Kohsuke× Sakamoto, Toshiaki× Kimura, Shinya× Tanimura, Susumu× Kohno, Michiaki |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Deregulated activation of protein tyrosine kinases, such as the epidermal growth factor receptor (EGFR) and Abl, is associated with human cancers including non-small cell lung cancer (NSCLC) and chronic myeloid leukemia (CML). Although inhibitors of such activated kinases have proved to be of therapeutic benefit in individuals with NSCLC or CML, some patients manifest intrinsic or acquired resistance to these drugs. We now show that, whereas blockade of either the extracellular signal-regulated kinase (ERK) pathway or the phosphatidylinositol 3-kinase (PI3K)-Akt pathway alone induced only a low level of cell death, it markedly sensitized NSCLC or CML cells to the induction of apoptosis by histone deacetylase (HDAC) inhibitors. Such enhanced cell death induced by the respective drug combinations was apparent even in NSCLC or CML cells exhibiting resistance to EGFR or Abl tyrosine kinase inhibitors, respectively. Co-administration of a cytostatic signaling pathway inhibitor may contribute to the development of safer anticancer strategies by lowering the required dose of cytotoxic HDAC inhibitors for a variety of cancers. | |||||
書誌情報 |
Biochemical and biophysical research communications 巻 391, 号 4, p. 1610-1615, 発行日 2010-01-22 |
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出版者 | ||||||
出版者 | Elsevier Inc. | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0006291X | |||||
EISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1090-2104 | |||||
書誌レコードID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA00564395 | |||||
PubMed番号 | ||||||
関連タイプ | isVersionOf | |||||
識別子タイプ | PMID | |||||
関連識別子 | 20026060 | |||||
DOI | ||||||
関連タイプ | isVersionOf | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1016/j.bbrc.2009.12.086 | |||||
権利 | ||||||
権利情報 | Copyright c 2009 Elsevier Inc. All rights reserved. | |||||
著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | Biochemical and biophysical research communications, 391(4), pp.1610-1615; 2010 |