| Project/Area Number |
26462535
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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 |
Obstetrics and gynecology
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| Research Institution | Wakayama Medical University |
|---|
Principal Investigator |
INO Kazuhiko 和歌山県立医科大学, 医学部, 教授 (60303640)
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| Co-Investigator(Kenkyū-buntansha) |
近藤 稔和 和歌山県立医科大学, 医学部, 教授 (70251923)
馬淵 泰士 和歌山県立医科大学, 医学部, 助教 (80382357)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 婦人科腫瘍 / 卵巣癌 / ケモカイン / 血管新生 / 免疫寛容 / ノックアウトマウス / 腫瘍免疫 / 腹膜播種 / 腫瘍微小環境 / マクロファージ |
|---|
| Outline of Final Research Achievements |
Interaction between tumor and stromal cells through chemokine systems was essential for cancer progression. The purpose of this study is to explore the pathophysiological roles of CX3CL1-CX3CR1 and CCR5 systems in ovarian cancer progression. A murine ovarian cancer cell line ID8 was used. When ID8 cells were inoculated to WT and Cx3cr1-/- mice, Cx3cr1-/- mice survived significantly longer than WT ones, and the tumor number in the abdominal cavity was significantly reduced in Cx3cr1-/- mice. Similarly, when ID8 cells were inoculated to WT and Ccr5-/- mice, tumor dissemination in abdominal cavity and tumor angiogenesis were significantly suppressed in Ccr5-/-mice compared with WT mice. These findings suggest that these chemokine networks are essential for ovarian cancer progression, and that CX3CR1 and CCR5 systems might be candidate molecules for a novel targeted therapy of ovarian cancer.
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