| Project/Area Number |
18K19464
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Review Section |
Medium-sized Section 50:Oncology and related fields
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
野口 雅之 筑波大学, 医学医療系, 教授 (00198582)
小島 崇宏 筑波大学, 医学医療系, 准教授 (40626892)
日下部 学 筑波大学, 医学医療系, 講師 (40804381)
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| Project Period (FY) |
2018-06-29 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
Fiscal Year 2019: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2018: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | がん微小環境 / がん免疫応答 / クローン造血 / マウスモデル / メラノーマ / TET2 / 炎症細胞 / 微小環境 |
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| Outline of Final Research Achievements |
Inflammatory cells having somatic mutations are thought to invade cancer tissues of patients with solid cancers accompanying clonal hematopoiesis. However, the roles of inflammatory cells with somatic mutations in the initiation and progression of cancers have not been clarified. In the present study, as a model for clonal hematopoiesis with TET2 mutations, B16 melanoma cell line was transplanted subcutaneously to the mice in which Tet2 gene was deficient in inflammatory cells of blood lineage (Tet2 deficient mouse) or control mice. Tumor formation was suppressed in Tet2-deficient mice. Bone marrow-derived suppressor cell and tumor-associated macrophage fractions were decreased in Tet2-deficient mice in the spleen. Since these cells are known to be involved in supporting tumor cells, reduction of these fractions may suppress the growth of melanoma.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究は、メラノーマモデルを用いることで、クローン造血を伴うがん患者のがん組織の微小環境について、体細胞変異のある炎症細胞という観点から解明する研究である。がんの微小環境を全く新しい視点から明らかにする点で、学術的に有意義である。クローン造血における体細胞変異とがんの組み合わせにより、炎症細胞の役割は多様であることが想定され、今後の研究の発展が期待される分野である。
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