@article{oai:kindai.repo.nii.ac.jp:00019876,
 author = {塩浜, 康雄 and Shihama,Yasuo and 藤田, 崇史 and Fujita,Takashi and 神武, 洋二郎 and Kotake,Yojiro and Demonacos, Constantinos and Krstic-Demonacos, Marija and Di Leva, Gianpiero and 藤井, 政幸 and Fujii,Masayuki},
 issue = {29},
 journal = {かやのもり：近畿大学産業理工学部研究報告, Reports of Faculty of Humanity-Oriented Science and Engineering, Kindai University},
 month = {Nov},
 note = {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., application/pdf},
 pages = {1--5},
 title = {〈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},
 year = {2018},
 yomi = {シハマ, ヤスオ and フジタ, タカシ and コウタケ, ヨウジロウ and フジイ, マサユキ}
}