| Project/Area Number |
15K10332
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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 |
Neurosurgery
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| Research Institution | Kobe University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
篠山 隆司 神戸大学, 医学部附属病院, 講師 (10379399)
田中 一寛 神戸大学, 医学研究科, 特定助教 (70467661)
水川 克 神戸大学, 医学部附属病院, 非常勤講師 (80403260)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | lymphoma / JAK / STAT / IL-10 / CNS / JAK-STAT / 中枢神経悪性リンパ腫 / STAT3 / primary CNS lymphoma |
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| Outline of Final Research Achievements |
Cerebrospinal fluid (CSF) interleukin-10 (IL-10) level was associated with activation level of JAK-STAT pathway in central nervous system lymphoma (PCNSL). PCNSL with high CSF IL-10 had strong expression of PIN-1 and SOCS, downstream molecules of JAK-STAT pathway. In addition, CSF IL-10 levels were associated with infiltration levels of tumor associated macrophages (TAMs) in PCNSL. When IL-10 protein was injected into inoculated subcutaneous PCNSL tumor of mouse, JAK and STAT3 in tumor cells was phosphorylated and activated by IL-10. But, JAK/STAT inhibitors could not show a antitumor effect in mouse models.
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