2017 Fiscal Year Final Research Report
Is the iPS marker "TRA-1-60" an indicator of cancer intractability against therapeutics?
| Project/Area Number |
16K15245
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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 |
Human pathology
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| Research Institution | Niigata University |
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Principal Investigator |
Kondo Eisaku 新潟大学, 医歯学系, 教授 (30252951)
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| Co-Investigator(Kenkyū-buntansha) |
奥田 修二郎 新潟大学, 医歯学系, 准教授 (00512310)
阪口 政清 岡山大学, 医歯薬学総合研究科, 准教授 (70379840)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Keywords | 膵がん / TRA-1-60 / PODXL1 / 転移 / 浸潤 |
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| Outline of Final Research Achievements |
1. PODXL1-konckout clones were generated from human three different PDAC lines since the TRA-1-60 is the glycosylated form of PODXL1. Consequently, drastic inhibition of liver metastasis in vivo was observed in all PODXL1-KO clone-xenografted mice generated from MiaPaCa-2, AsPC1, Panc-1.
2. PODXL1 revealed to form complex with multiple cytokine receptors and its binding contribute to activate those receptors.
3. PODXL1 was highly expressed at the invasive front and metastatic foci of PDAC cells in patients' tumor tissues.
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| Free Research Field |
腫瘍病理学
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