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自然免疫応答の賦活化を基盤とした膵癌新規薬物併用療法の開発
https://doi.org/10.24517/00050722
https://doi.org/10.24517/00050722215bd56d-7698-441c-8582-def106e70223
名前 / ファイル | ライセンス | アクション |
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HO-PR-OHTA-T-kaken 2016-4p.pdf (293.5 kB)
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Item type | 報告書 / Research Paper(1) | |||||
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公開日 | 2018-05-14 | |||||
タイトル | ||||||
タイトル | 自然免疫応答の賦活化を基盤とした膵癌新規薬物併用療法の開発 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | Low-dose gemcitabine induces major histocompatibility complex class I-related chain A/B expression and enhances an antitumor innate immune response in pancreatic cancer | |||||
言語 | ||||||
言語 | jpn | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_18ws | |||||
資源タイプ | research report | |||||
ID登録 | ||||||
ID登録 | 10.24517/00050722 | |||||
ID登録タイプ | JaLC | |||||
著者別表示 |
Ohta, Tetsuo
× Ohta, Tetsuo |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学医薬保健研究域医学系 | |||||
書誌情報 |
平成27(2015)年度 科学研究費補助金 基盤研究(C) 研究成果報告書 en : 2015 Fiscal Year Final Research Report 巻 2013-04-01 - 2016-03-31, p. 4p., 発行日 2016-06-18 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | 自然免疫逃避機構に関与する腫瘍のMIC(MHC classⅠrelated chain)A/B発現の増強効果に着目した。切除標本を用いた検討にて術前化学療法(Gemcitabine:GEM)を施行すると癌細胞のMICA発現が増強し、周囲に免疫担当細胞の浸潤が高率に認められた。また膵癌細胞株を用いた検討では低濃度GEMにValpronic acid(VPA)を付加すると、MICA/Bの発現が増強され、またγδT細胞による傷害活性の向上が認められた。さらに可溶性MICA/Bの増加を抑制することが示された。以上よりGEM+VPA療法は免疫逃避機構を解除する可能性が示唆される。 | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | We investigated the effect of gemcitabine (GEM), a key drug for pancreatic cancer treatment, on the expression of cell surface MICA/B in pancreatic cancer cells and resulting cytotoxicity of γδ T cells. MICA and CD16 expressions from resected pancreatic cancer patient specimens, which received neoadjuvant chemotherapy (NAC) with GEM, were analyzed by immunohistochemistry. Immunohistochemical staining demonstrated that MICA expression in tumor cells and CD16 positive cells surrounding tumors were significantly higher in the NAC group compared to that of the control group. The present results indicate that low-dose GEM-induced MICA/B expression enhances innate immune function rather than cytotoxicity in pancreatic cancer. In addition, our result suggests that the inhibition of cleavage and release of MIC molecules from the tumor surface could potentially improve NKG2D-dependent cytotoxicity. | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 研究課題/領域番号:25462106, 研究期間(年度):2013-04-01 - 2016-03-31 | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 出典:研究課題「自然免疫応答の賦活化を基盤とした膵癌新規薬物併用療法の開発」課題番号25462106 (KAKEN:科学研究費助成事業データベース(国立情報学研究所)) (https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-25462106/25462106seika/)を加工して作成 |
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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 | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/search/?qm=40194170 | |||||
関連名称 | https://kaken.nii.ac.jp/search/?qm=40194170 | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-25462106/ | |||||
関連名称 | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-25462106/ | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-25462106/25462106seika/ | |||||
関連名称 | https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-25462106/25462106seika/ |