| Project/Area Number |
18K16736
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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 56030:Urology-related
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| Research Institution | Tottori University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2020: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 腎細胞癌 / スニチニブ耐性 / microRNA / スニチニブ抵抗性 / アキシチニブ抵抗性 / バイオマーカー / LAMP-2 / 分子標的薬 / 免疫チェックポイント阻害薬 |
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| Outline of Final Research Achievements |
In the sunitinib resistance model (SR-ACHN) compared to the human RCC cell line ACHN, the expression of all three splice variants of lysosome-associated membrane protein 2 (LAMP-2), LMP-2A, 2B and 2C, was found to be elevated. However, cytotoxicity studies in forced-expression strains confirmed that forced-expression strains of LAMP-2A and 2B were significantly more resistant to sunitinib compared to ACHN. Taken together, these results indicate that LAMP-2A and LAMP-2B are involved in sunitinib resistance in RCC.
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| Academic Significance and Societal Importance of the Research Achievements |
近年、進行性腎癌の薬物療法においてスニチニブが使用される機会は減少したが、その他のチロシンキナーゼ阻害薬は1次併用療法の一剤として使用頻度が高い。本研究の成果は、そのようなチロシンキナーゼ阻害薬に対する薬剤耐性メカニズムの解明の一助となる可能性がある。
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