| Project/Area Number |
23590409
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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 |
Human pathology
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| Research Institution | Jichi Medical University |
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Principal Investigator |
DOBASHI Yoh 自治医科大学, 医学部, 准教授 (90231456)
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| Co-Investigator(Kenkyū-buntansha) |
ENDO Shunsuke 自治医科大学, 医学部, 教授 (10245037)
YANAGAWA Takashi 群馬大学, 医学部, 講師 (40400725)
KITAGAWA Masatoshi 浜松大学, 医学部, 教授 (50294971)
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| Co-Investigator(Renkei-kenkyūsha) |
MATSUBARA Hirochika 山梨大学, 医学部, 講師 (00374166)
OOI Akishi 金沢大学, 医学系研究科, 教授 (50160411)
HARUHIKO Sugimura 浜松医科大学, 医学部, 教授 (00196742)
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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: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 肺癌 / 骨軟部肉腫 / AKT / mTOR / 遺伝子増幅 / 遺伝子多型 / シグナル伝達 / Akt / 骨軟部腫瘍 / microRNA / microarray / 遺伝子変異 |
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| Research Abstract |
In lung carcinomas and soft tissue sarcomas, Akt expression/activation, and AKT1-3 gene gains were investigated. In lung carcinomas, immunohistochemistry revealed expression of Akt in 60% and phosphorylated-Akt (p-Akt), Akt1, Akt2 in 40%, but expression of Akt3 was lower as 20% in approximate. A significant correlation between Akt2/p-Akt expression and lymph node metastasis was observed. In sarcomas, the cases showing activated Akt/mTOR pathway revealed worse prognosis in several histological types. FISH analysis indicated "FISH-positive" gene gain (amplification/high level polysomy) of AKT1/2 in 15 to 25% in both tumors. FISH-positive AKTs gene gain accompanied activation of Akt, but not EGFR gains. Microarray analysis revealed that AKT1/2 gene increase induced specific mRNA and microRNA, which are known to be involved in invasion or epithelial-mesenchymal transition. Moreover, a polymorphic site in AKT1 related to cancer predisposition was identified by SNP analysis.
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