| Project/Area Number |
17K16849
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Osaka University |
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Principal Investigator |
Matsumoto Yuri 大阪大学, 医学部附属病院, 助教 (90756488)
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| Research Collaborator |
Kozasa Katsumi
Yokoi Eriko
Komura Naoko
Shimura Koutaro
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 子宮体癌 / TAN / CXCL2 / E2 / MDSC / 好中球増多 / CXCL8 / STAT6 / HIF-1 |
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| Outline of Final Research Achievements |
The aim of this study was to find out the new treatment that specifically inhibit TAN (tumor-associated neutrophil) in endometrial cancer displaying tumor-related neutrophilia by identifying the mechanism by which neutrophils infiltrate into cancer tissue and the mechanism of neutrophil differentiation into TAN. We identified that cancer cells secreted CXCL2, which cause chemotaxis by attracting neutrophils that express CXCR2, an express CXCL2 receptor. Moreover, we demonstrated that granulocytic MDSC (myeloid-derived suppressor cell), which are believed to be close to or the same as TAN, was differentiated by 17β-estradiol (E2). We are currently investigating the efficacy and safety of new treatment for endometrial cancer that is targeted at CXCL2 and E2.
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| Academic Significance and Societal Importance of the Research Achievements |
好中球増多を伴う子宮体癌は標準治療に抵抗性を示し予後不良であり、その原因のひとつでことが証明されている TAN の分化のメカニズムを明らかにしたことで、TANを特異的に阻害する新規治療の開発に向けて大きな意義があると考えられる。好中球増多は、子宮体癌以外の悪性腫瘍にとっても、重要な予後因子であることも報告されており、本研究の成果は好中球増多を伴う他の癌種へ応用することも可能と考えられ、その医学的意義は非常に大きいと考える。
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