| Project/Area Number |
15K15603
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Nagoya University |
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Principal Investigator |
Iwase Akira 名古屋大学, 医学部附属病院, 病院教授 (20362246)
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| Co-Investigator(Kenkyū-buntansha) |
中村 智子 名古屋大学, 医学部附属病院, 助教 (40732681)
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| Research Collaborator |
ISHIDA Chiharu 名古屋大学, 大学院医学系研究科, 大学院生
NAGAI Takashi 名古屋大学, 大学院医学系研究科, 大学院生
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 子宮内膜症 / 卵巣癌 / チョコレート嚢胞 / 腹膜播種 / Focal adhesion kinase / チョコレートのう胞 |
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| Outline of Final Research Achievements |
Endometriosis and ovarian cancer often cause relatively big ovarian cystic lesions and small disseminated lesions on peritoneum. We focused on the common features of endometriosis and ovarian cancer and explored interrelation between tumorigenesis and tumor microenvironments.
We found the production of monocyte chemotactic protein-1 and transforming growth factor-β from endometriotic stromal cells induce by the adhesion onto extracellular matrix that was inhibited by focal adhesion kinase（FAK）inhibitor. Our results indicated the significance of FAK-mediated signaling in two distinguished features of endometriosis, local inflammation and fibrosis. FAK can be a therapeutic target of endometriosis.
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