| Project/Area Number |
23390221
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Okayama University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TKIGAWA Nagio 川崎医科大学, 医学部, 教授 (60325107)
HOTTA Katsuyuki 岡山大学, 大学病院, 講師 (70379816)
市原 英基 岡山大学, 医歯(薬)学総合研究科, 講師 (40549705)
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| Co-Investigator(Renkei-kenkyūsha) |
TAKATA Minoru 京都大学, 放射線生物研究センター, 教授 (30281728)
NAKABEPPU Yusaku 九州大, 学生体防御医学研究所, 教授 (30180350)
YOSHINO Tadashi 岡山大学, 医薬歯学総合研究科, 教授 (70183704)
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| Project Period (FY) |
2011-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥19,500,000 (Direct Cost: ¥15,000,000、Indirect Cost: ¥4,500,000)
Fiscal Year 2014: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2011: ¥8,190,000 (Direct Cost: ¥6,300,000、Indirect Cost: ¥1,890,000)
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| Keywords | EGFR遺伝子改変マウス / afatinib / everolimus (mTOR阻害薬), / JAK-1/2 inhibitors / cetuximab / bevacizumab / Ogg1ホモノックアウトマウス / NNK / EGFR / everolims / AZD1480 / gefitinib / 用量依存性 / 遺伝子改変マウス / ｍTOR阻害薬 / everolimus / JAK1/2阻害薬 / BIBW2552 / mTOR阻害薬 |
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| Outline of Final Research Achievements |
① Using the EGFR genetically modified mice, afatinib (irreversible TKI), everolimus (mTOR inhibitor), and AZD1480 (JAK-1/2 inhibitors) revealed an anti-tumor effect. ②In mouse xenograft models, afatinib + cetuximab + bevacizumab combination therapy against resistant cells harbouring T790M has proved to result in lasting pathologic complete response. ③ Although 9.3% of Ogg1 (-/-) homozygous knockout mice to a high dose of tobacco-specific nitrosamines (NNK) had adenocarcinoma of the lung, it is not recognized carcinogenesis at low doses. The relationship between epidermal growth factor receptor (EGFR) gene mutations and NNK-induced carcinogenesis was unclear.
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