| Project/Area Number |
25293284
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Department of Clinical Research, National Hospital Organization Kure Medical Center (2016)
Hiroshima University (2013-2015) |
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Principal Investigator |
Hinoi Takao 独立行政法人国立病院機構(呉医療センター臨床研究部), その他部局等, 臨床研究部室長 (10444689)
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| Co-Investigator(Renkei-kenkyūsha) |
SOTOMARU Yusuke 広島大学, 自然科学研究支援開発センター, 教授 (90309352)
IKENOUE Tsuneo 東京大学, 医科学研究所, 准教授 (80396712)
OUE Naohide 広島大学, 医歯薬保健学研究院, 准教授 (60346484)
TOMONAGA Takeshi 独立行政法人医薬基盤研究所, プロジェクトリーダー (80227644)
OHDAN Hideki 広島大学, 医歯薬保健学研究院, 教授 (10363061)
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| Research Collaborator |
ADACHI Tomohiro
SAITO Yasufumi
MIGUCHI Masashi
NIITSU Hiroaki
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥17,810,000 (Direct Cost: ¥13,700,000、Indirect Cost: ¥4,110,000)
Fiscal Year 2016: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2013: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
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| Keywords | 大腸癌 / マウスモデル / バイオマーカー / RAS / TGFbetaRII / Kras / TGFbeta / 遺伝子改変マウス / 大腸癌マウスモデル / KRAS変異型大腸癌 / MSI大腸癌マウスモデル |
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| Outline of Final Research Achievements |
We applied two types of genomic instability in advanced colon cancer mouse model (colonic epithelial cell specific conditional Apc-knockout mouse) that we established and added another carcinogen driver gene (Kras, TGFβIIR)mutation to Apc mutation to generate complex genetically modified mouse model. The tumor of Apc+Kras mutant mouse was moderately differentiated adenocarcinoma and by comprehensive gene analysis Glut1 and Rcan2 were identified as upregulated and downregluated target genes, respectively. In Apc + TGFβIIRk deficient mice, the expression of GSDMC transcript and protein was elevated. From these mice models, biomarkers useful for treatment such as correlation of genotype-phenotype of oncogenic driver gene and target gene could be identified.
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