Item type |
itemtype_ver1(1) |
公開日 |
2021-12-03 |
タイトル |
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タイトル |
S-1 facilitates canerpaturev (C-REV)-induced antitumor efficacy in a triple-negative breast cancer model |
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言語 |
en |
著者 |
Miyajima, Noriyuki
Ragab Eissa, Ibrahim
Abdelmoneim, Mohamed
Naoe, Yoshinori
Ichinose, Toru
Matsumura, Shigeru
Bustos-Villalobos, Itzel
Mukoyama, Nobuaki
Morimoto, Daishi
Shibata, Masahiro
Takeuchi, Dai
Tsunoda, Nobuyuki
Kikumori, Toyone
Tanaka, Maki
Kodera, Yasuhiro
Kasuya, Hideki
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アクセス権 |
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アクセス権 |
open access |
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アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
権利 |
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言語 |
en |
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権利情報Resource |
http://creativecommons.org/licenses/by-nc-nd/4.0/ |
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権利情報 |
Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International |
キーワード |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
oncolytic virus |
キーワード |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
canerpaturev |
キーワード |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
S-1 |
キーワード |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
myeloid-derived suppressor cells |
内容記述 |
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内容記述タイプ |
Abstract |
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内容記述 |
Canerpaturev (C-REV) is a highly attenuated, replication-competent, mutant strain of oncolytic herpes simplex virus type 1 that may be an effective new cancer treatment option. S-1, an oral formulation containing the 5-fluorouracil (5-FU) prodrug tegafur and the two enzyme modulators gimeracil and oteracil, is used as a key chemotherapeutic agent for metastatic recurrent breast cancer. Although the antitumor effects of oncolytic viruses combined with 5-FU in vivo have been reported, the detailed mechanisms are unknown. Here, we investigated the antitumor mechanism of the combination of C-REV and S-1 in triple-negative breast cancer (TNBC) in the context of tumor immunity. The combined effect of C-REV and S-1 was evaluated in a bilateral tumor model of murine TNBC 4T1 in vivo. S-1 enhanced the TNBC growth inhibitory effects of C-REV, and decreased the number of tumor-infiltrating, myeloid-derived suppressor cells (MDSCs), which suppress both innate and adaptive immune responses. Moreover, C-REV alone and in combination with S-1 significantly increased the number of CD8+ T cells in the tumor and the production of interferon γ (IFNγ) from these cells. Our findings indicate that C-REV suppresses TNBC tumor growth by inducing the expansion of effector CD8+ T cell subsets in tumors in which S-1 can inhibit MDSC function. Our study suggests that MDSCs may be an important cellular target for breast cancer treatment. The combination of C-REV and S-1 is a new approach that might be directly translated into future clinical trials against TNBC. |
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言語 |
en |
出版者 |
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出版者 |
Nagoya University Graduate School of Medicine, School of Medicine |
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言語 |
en |
言語 |
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言語 |
eng |
資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
departmental bulletin paper |
出版タイプ |
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出版タイプ |
VoR |
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出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
ID登録 |
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ID登録 |
10.18999/nagjms.83.4.683 |
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ID登録タイプ |
JaLC |
関連情報 |
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関連タイプ |
isVersionOf |
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識別子タイプ |
URI |
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関連識別子 |
https://www.med.nagoya-u.ac.jp/medlib/nagoya_j_med_sci/834.html |
助成情報 |
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助成機関名 |
日本学術振興会 |
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言語 |
ja |
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助成機関名 |
Japan Society for the Promotion of Science |
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言語 |
en |
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研究課題番号URI |
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16H05413/ |
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研究課題番号 |
16H05413 |
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研究課題名 |
HF10ウイルスの抗腫瘍効果における新たな免疫因子の役割 |
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言語 |
ja |
助成情報 |
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助成機関名 |
日本学術振興会 |
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言語 |
ja |
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助成機関名 |
Japan Society for the Promotion of Science |
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言語 |
en |
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研究課題番号URI |
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16K15611/ |
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研究課題番号 |
16K15611 |
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研究課題名 |
革新的な腫瘍抗原ウイルスとTCR遺伝子改変T細胞の併用療法の開発 |
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言語 |
ja |
収録物識別子 |
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収録物識別子タイプ |
PISSN |
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収録物識別子 |
0027-7622 |
収録物識別子 |
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収録物識別子タイプ |
EISSN |
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収録物識別子 |
2186-3326 |
書誌情報 |
en : Nagoya Journal of Medical Science
巻 83,
号 4,
p. 683-696,
発行日 2021-11
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