| Project/Area Number |
23592954
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | Tohoku University |
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Principal Investigator |
SHINOHARA FUMIAKI 東北大学, 歯学研究科(研究院), 大学院非常勤講師 (80400258)
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| Co-Investigator(Kenkyū-buntansha) |
MIYASHITA Hitoshi 東北大学, 歯学研究科, 助教 (70372323)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
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| Keywords | 口腔癌 / 上皮増殖因子 / 分子標的薬 / インターフェロンガンマ / 上皮成長因子 / 癌 / 抗癌剤 / EGFR |
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| Research Abstract |
In the present study, we evaluated the combination chemotherapy for oral cancer using anti-cancer agents (5-FU and CDDP) and the molecular target reagent, Cetuximab which is an antagonist of epidermal growth factor receptor (EGFR). We also analyzed the mechanism how the enzymes, which express on tumor cells and play as an IFNG degrading enzyme, affect circumvention of tumor immunity. Our results suggest that Cetuximab inhibits Akt and autophagy resulting in the up-regulation of apoptosis induced by 5-FU. IFNG concentration was decreased in the culture supernatant of each cell line and the difference of mRNA expression of TACE was observed among cell lines. Mass spectrometry analysis indicated that TACE, other enzymes and KRAS gene were involved in the degradation of IFNG.
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