| Project/Area Number |
16K09325
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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 |
Gastroenterology
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| Research Institution | Keio University |
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Principal Investigator |
Matano Mami 慶應義塾大学, 医学部(信濃町), 研究員 (20439889)
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| Co-Investigator(Kenkyū-buntansha) |
佐藤 俊朗 慶應義塾大学, 医学部(信濃町), 教授 (70365245)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 大腸癌 / オルガノイド / 大腸がん / 癌 |
|---|
| Outline of Final Research Achievements |
The factors contributing in the malignant transformation process of normal colon epithelium are still unknown. The genetically-engineered normal colon organoids in our laboratory did not develop into a colorectal cancer, suggesting the involvement of additional factors. We assumed the involvement of the epigenetic changes and aimed to identify the transcription factors. To identify the transcription factors, we extracted the transcription factors using our database of colorectal cancer organoids, and constructed the overexpression vectors. We introduced them into genetically-engineered normal colon organoids and transplanted to mice to evaluate the presence of liver metastasis. Consequently, no liver metastasis were observed with any combination of transcription factors, and we concluded that further study is required.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究結果の学術的意義は, 今回我々が選択した転写因子だけでは既存の大腸発癌の理論を補完・再現するには不十分である可能性が示唆されたことである. 本成果より, 今回着目した転写因子の変動をきたす, より根源的原因の探索の必要性が考えられた. 社会的意義として, その根源的原因が今後の治療標的となる可能性が示唆された.
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