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〈論文・報告〉Gapmerアンチセンス核酸による変異癌遺伝子KRAS(G12D)の選択的発現制御
https://doi.org/10.15100/0000019876
https://doi.org/10.15100/0000019876dc0fc959-86f1-473c-a73c-0b383b25eaa6
名前 / ファイル | ライセンス | アクション |
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AA12013209-20181130-0001.pdf (1.4 MB)
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Item type | ☆紀要論文 / Departmental Bulletin Paper(1) | |||||
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公開日 | 2019-01-28 | |||||
タイトル | ||||||
言語 | ja | |||||
タイトル | 〈論文・報告〉Gapmerアンチセンス核酸による変異癌遺伝子KRAS(G12D)の選択的発現制御 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | 〈PAPERS and REPORTS〉Selective Regulation of Mutant Oncogene KRAS (G12D) by Gapmer Antisense Nucleic Acids | |||||
著者 |
塩浜, 康雄
× 塩浜, 康雄× 藤田, 崇史× 神武, 洋二郎× Demonacos, Constantinos× Krstic-Demonacos, Marija× Di Leva, Gianpiero× 藤井, 政幸 |
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言語 | ||||||
言語 | jpn | |||||
キーワード | ||||||
主題 | Mutant KRAS Positive Cancer, Nucleic Acid Therapeutics, Gapmer Antisense Oligonucleotides | |||||
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 | |||||
ID登録 | ||||||
ID登録 | 10.15100/0000019876 | |||||
ID登録タイプ | JaLC | |||||
著者 所属 | ||||||
近畿大学産業理工学部生物環境化学科; 博士研究員 | ||||||
著者 所属 | ||||||
近畿大学産業理工学部生物環境化学科 | ||||||
著者 所属 | ||||||
近畿大学産業理工学部生物環境化学科; 教授 | ||||||
著者 所属 | ||||||
マンチェスター大学; 教授 | ||||||
著者 所属 | ||||||
サルフォード大学; 教授 | ||||||
著者 所属 | ||||||
サルフォード大学; 教授 | ||||||
著者 所属 | ||||||
近畿大学産業理工学部生物環境化学科; 教授 | ||||||
版 | ||||||
出版タイプ | NA | |||||
出版タイプResource | http://purl.org/coar/version/c_be7fb7dd8ff6fe43 | |||||
出版者 名前 | ||||||
出版者 | 近畿大学産業理工学部 | |||||
書誌情報 |
ja : かやのもり:近畿大学産業理工学部研究報告 en : Reports of Faculty of Humanity-Oriented Science and Engineering, Kindai University 号 29, p. 1-5, 発行日 2018-11-30 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 13495801 | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | KRAS mutation is positive in 45% of colon cancer patients, 35% of lung cancer patients, 95% of pancreas cancer patients, and 15% of melanoma patients and the patients do not benefit from anti-epidermal growth factor receptor (EGFR) chemotherapy and antibody therapy to have poor prognosis for survival. KRAS mutations in codons 12 and 13 were present approximately in 40% of colorectal cancers. It is highly challenging to target mutant KRAS gene by synthetic small nucleic acids and can be a breakthrough for undruggable cancers.In the present study, we investigated silencing efficiencies of mutant KRAS(G12D) gene by gapmer antisense oligonucleotides (ASO) using HeLa with wild type KRAS and PK-45H with G12D mutation in both alleles. ASOs targeting mutant KRAS (G12D) with 11nt and 9nt phosphorothioate gap silenced KRAS(G12D) expression in 81% and 73% efficiency in PK-45H, respectively but affected very little on the wild type KRAS expression in HeLa. | |||||
言語 | en | |||||
フォーマット | ||||||
内容記述タイプ | Other | |||||
内容記述 | application/pdf |