| Project/Area Number |
15K08654
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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 |
Laboratory medicine
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| Research Institution | Tokai University |
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Principal Investigator |
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| Research Collaborator |
DAMDINSUREN Anar 東海大学, 医学部, 研究員
NEMEKHBAATAR Lkhaasuren 東海大学, 医学部, 研究員
TSEVEGJAV Bayarbat 東海大学, 医学部, 研究員
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 白血病 / 治療抵抗性 / 抗がん剤 / 骨髄微小環境 / FLT3-ITD / 遺伝子診断 / 急性骨髄性白血病 / 遺伝子変異 / チロシンキナーゼレセプター / 骨髄間質細胞 / 遺伝子 |
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| Outline of Final Research Achievements |
This study was conducted to clarify molecular mechanisms of refractory leukemia cells in the bone marrow microenvironment. When FLT3-ITD positive leukemia cell lines (either exogenous or endogenous, K562 or MOLM-14, MV4:11, respectively) were cultured in the presence of components of extracellular matrix, such as fibronectin, of the bone marrow microenvironment, Ara-C resitance was significantly and specifically enhanced. Genes coding fibronectin or its receptor are increased in the expression at the interaction. These findings would be a part of molecular mechanisms of refractory leukemia cells in the bone marrow microenvironment after chemotherapy. The involved genes and signals would contributory to biomarkers relevant for diagnosis and monitoring the disease.
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