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

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Author: 太田, 哲生ほか

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Publication date: 2016-06-18

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Note (General)：: 金沢大学医薬保健研究域医学系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...

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https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-25462106/25462106seika/

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Material Type: 文書・図像類
Title: 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
Author/Editor: 太田, 哲生
Ohta, Tetsuo
Author Heading: 太田, 哲生
Ohta, Tetsuo
Publication Date: 2016-06-18
Publication Date (W3CDTF): 2016-06-18
Alternative Title: Low-dose gemcitabine induces major histocompatibility complex class I-related chain A/B expression and enhances an antitumor innate immune response in pancreatic cancer
Periodical title: 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 = 2015 Fiscal Year Final Research Report
No. or year of volume/issue: 2013-04-01 - 2016-03-31
Volume: 2013-04-01 - 2016-03-31
Pages: 4p.-
Text Language Code: jpn
Subject Heading: 膵癌
術前化学療法
免疫逃避機構
MICA/B
Gemcitabine
Valpronic acid
自然免疫機構
Target Audience: 一般
Note (General): 金沢大学医薬保健研究域医学系
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。
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.
研究課題/領域番号:25462106, 研究期間(年度):2013-04-01 - 2016-03-31
DOI: 10.24517/00050722
Source: https://kanazawa-u.repo.nii.ac.jp/?action=repository_action_common_download&item_id=44380&item_no=1&attribute_id=26&file_no=1
https://kanazawa-u.repo.nii.ac.jp/?action=repository_action_common_download&item_id=44380&item_no=1&attribute_id=26&file_no=1
Access Restrictions: 限定公開
Rights (production): CC BY-NC-ND
Related Material: https://kaken.nii.ac.jp/search/?qm=40194170
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-25462106/
https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-25462106/25462106seika/
Data Provider (Database): 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
Original Data Provider (Database): 金沢大学 : 金沢大学学術情報リポジトリKURA