| Project/Area Number |
18K15210
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 50010:Tumor biology-related
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Ito Kenji 東京大学, 医科学研究所, 特任研究員 (20757504)
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ゲノム核内構造 / 遺伝子変異 / 発がん / エピジェネティクス / 老化 / 核内構造 / がん / 発がんモデル |
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| Outline of Final Research Achievements |
During the period of this research project, we established a doxycycline-inducible clear cell sarcoma model mouse capable of inducing oncogene expression in various types of tissue. By using this mouse, we uncovered (1) Oncogene Induced Senescence (OIS) has occurred in most cell types, and (2) avoidance of OIS and cancer development have occurred only in soft tissue. We also clarified that the change in chromatin structure formed by the transcription factor expressed in the cell of origin of clear cell sarcoma is the mechanism behind the tissue-specific cancer development. This work was published from Nature Communications (Komura S *, Ito K *, Nature Com., 2019).
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| Academic Significance and Societal Importance of the Research Achievements |
近年、細胞老化は発がんの抑制に関与しうる事が報告されている。したがって、本研究成果はゲノム核内構造の変換を伴うクロマチン構造の変化に着目し、それをマウス個体内で誘導する事で細胞老化を誘導し、発がんを抑制出来る可能性を示したという点において意義深いと言える。
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