| Project/Area Number |
17K18205
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cell biology
Hematology
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | スフィンゴミエリン / スフィンゴミエリン合成酵素 / 急性骨髄性白血病 / 腫瘍免疫 / スフィンゴ脂質 / 細胞障害性T細胞 / sphingomyelin synthase / acute myeloid leukemia / sphingomyelin / CTL / MDSC / sphingolipid / cancer progression |
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| Outline of Final Research Achievements |
Acute myeloid leukemia (AML) is the cancer of hematopoietic myeloid cells induced by genomic mutation. Organisms eliminates cancer cells through activation of tumor immunity. However, cancer cells also have the ability of cancer immunoediting and suppress tumor immunity cells. Sphingomyelin (SM) is the main constitution of lipid bilayer membrane and regulates the signal transduction through affecting ligand-receptor association or cell-cell adhesion, which are involved in the inflammatory and its-mediated immune responses. However, it is unclear that the involvement of SM and SM production by SM synthase (SMS) in the regulation of tumor immunity or cancer immunoediting. In this study, I showed that deficiency of SMS suppresses AML through activation of tumor immunity.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究成果はスフィンゴミエリン合成酵素の欠損により腫瘍免疫の活性化を介して急性骨髄性白血病が抑制されることから、スフィンゴミエリン合成酵素ががん抑制の標的となり得ることを示唆しており、がんの治療法の開発へと繋がる研究基盤となることが期待できる。
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