@techreport{oai:kindai.repo.nii.ac.jp:00019763,
 author = {武田, 真幸},
 month = {},
 note = {研究成果の概要（和文）：2013年7月～2015年3月に近畿大学で診断された肺癌110例を前向きに解析しホルマリン固定パラフィン包埋腫瘍検体からDNA, RNA抽出後遺伝子変異解析実施例は、それぞれ95％、96％と高率で実施可能であった。少なくとも1つ以上のアミノ酸置換を生じる遺伝子変異は69％の症例に認められ、薬剤感受性に関与するActionable遺伝子変異は40%に同定され、Actionable遺伝子変異有り且つ分子標的薬導入群は、変異無し群、及び、Actionable遺伝子遺伝子変異有り且つ分子標的薬導入無し群と比較し、有意に全生存期間を延長することを示しマルチ遺伝子パネルの臨床的有用性を示すことができた。
研究成果の概要（英文）：Tumor specimens from 110 patients with lung cancer recruited between July 2013 and March 2015 were analyzed. The most common genetic alterations were TP53 mutations in 42 patients, followed by EGFR mutations in 25, STK11 mutations in 12, and KRAS mutations in 10.Potentially actionable mutations were identified in 44 patients including 50% of those with adenocarcinoma and 14% of those with squamous cell carcinoma. The OS of patients with advanced or recurrent cancer who had an actionable mutation and received targeted therapy (median OS not achieved) was significantly longer than that of those with no mutation (18.1 months, P = 0.041) or of those with a mutation not so treated (6.1 months, P = 0.0027).Multiplex genomic testing was performed on formalin-fixed, paraffin-embedded tumor specimens with a success rate of -95%. Such testing can assist physicians in matching patients with approved or experimental targeted treatments., 研究種目：若手研究(B);  研究期間：2015～2017;   課題番号：15K21525;   研究分野：臨床腫瘍学;   科研費の分科・細目：, application/pdf},
 title = {ドライバー遺伝子肺癌の薬剤感受性メカニズムの解明},
 year = {2018},
 yomi = {タケダ, マサユキ}
}