| Project/Area Number |
16K11013
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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 |
Urology
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| Research Institution | Kumamoto University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
河野 吉昭 熊本大学, 大学院生命科学研究部(医), 講師 (30593793)
菰原 義弘 熊本大学, 大学院生命科学研究部(医), 准教授 (40449921)
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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 |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 腎細胞癌 / 癌免疫 / マクロファージ / TIMD4 / 免疫療法 / 腎癌 |
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| Outline of Final Research Achievements |
We tested if TAM or TAM-rated molecules would be associate clinicopathological factors or cancer progression. PD-L1 expression in papillary RCC was detected, however, no significant correlation with clinicopathological factors were seen. This study was first report described the PD-L1 expression in papillary RCC. TIMD4 and CD163-positive cancer cells were observed in clear cell RCC, and positive cases showed poor clinical course. TIMD4 was suggested to be involved in chemo-resistance by means of in vitro study using RCC cell lines. TAM phenotype between primary RCC and metastatic RCC was tested, and M1-like TAMs were suggested to be increased in metastatic site.
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| Academic Significance and Societal Importance of the Research Achievements |
腎癌においてTAMあるいはTAM関連分子の重要性を明らかにした。予後予測因子やあらたな治療法開発につながるように今後も研究を続けていきたい。
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