| Project/Area Number |
23590406
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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 |
Human pathology
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| Research Institution | Yokohama City University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Reiko 千葉大学, 真菌医学研究センター, 助教 (60143319)
AOKI Ichiro 横浜市立大学, 医学研究科, 教授 (00184028)
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| Co-Investigator(Renkei-kenkyūsha) |
MIYAGI Etsuko 横浜市立大学, 附属病院, 准教授 (40275053)
MIYAGI Yohei 神奈川県立がんセンター, がん分子病態研究部門, 部門長 (00254194)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 卵巣癌 / 炎症 / ケモカイン / 炎症性微小環境 / シグナル / 発癌 / 人体病理 |
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| Research Abstract |
We examined pathophysiology of impaired CXCR3 signaling in endometriosis-associated ovarian cancer (EAOC) under IFN-g enriched microenvironment.
The expression of CXCL4, a ligand of CXCR3-B, was gradually suppressed as cancer developed from endometriosis lesion. We confirmed that the responsible cell type expressing CXCL4 was macrophage. Interestingly, infiltrating macrophages in endometriosis were CD68 (+) CXCL4 (+) whereas those in EAOC were CD163 (+) CXCL4 (-). Furthermore, we found that suppressor of cytokine signaling (SOCS) was severely suppressed in these IFN-g-high EAOC.
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