| Project/Area Number |
12671548
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Urology
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
TAKAHASHI Atsushi (2001-2002) Sapporo Medical University School of Medicine, Assistant Professor, 医学部, 講師 (20274946)
柳瀬 雅裕 (2000) 札幌医科大学, 医学部, 助手 (80291558)
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| Co-Investigator(Kenkyū-buntansha) |
YANASE Masahiro Sapporo Medical University School of Medicine, Senior Instructor, 医学部, 助手 (80291558)
TSUKAMOTO Taiji Sapporo Medical University School of Medicine, Professor, 医学部, 教授 (50112454)
高橋 敦 札幌医科大学, 医学部, 助手 (20274946)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2002: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2001: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2000: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | RCC / cytokine / VEGF / FLT-3 / 樹状細胞 / FLT-3-ITD / FLT-3阻害薬 / FLT-3リガンド / 免疫療法 / RCC / IL-6 |
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| Research Abstract |
1) Recent reports showed that vascular endothelial growth factor (VEGF) and interleukin-6 (IL-6) might be involved to defective function of dendritic cells, leading to poor prognosis due to failure of immunotherapy. To test hypothesis, we measured serum levels of VEGF and IL-6 in RCC patients. Patients with elevated levels of VEGF and IL-6 had worse prognosis, suggesting that these factors (VEGF and IL-6) might affect dendritic cell dysfunction.
2) Among various factors which induce and proliferation and differentiation of dendritic cells, we focused on FLT-3 ligand-FLT-3 pathway, because interestingly FLT-3 is expressed in RCC cell lines. FLT-3 ligand did not affect the cell growth in RCC cell lines in vitro. About 20-30% of acute myeloid leukemia patients show genetic mutations of FLT-3, which leads to constitutive activation of FLT-3 activity. We hypothesized a similar mechanism as cause of fFLT-3 expression in RCC. However, no mutation was seen in RCC cell lines, indicating other mechanism than known mutation of FLT-3. The protein kinase inhibitor SU5614 failed to inhibit the cell growth to RCC cell lines in vitro. However, FLT-3 might be still a new target for treating RCC patients.
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