| Project/Area Number |
26460439
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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 | Kitasato University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
堀江 良一 北里大学, 医療衛生学部, 教授 (80229228)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ホジキンリンパ腫 / CD30 / Epstein-Barr virus (EBV) / リンパ芽球様細胞株 (LCL) / EB ウイルス / CD0 / Hodgkinリンパ腫 / EBウイルス |
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| Outline of Final Research Achievements |
In this study we aimed to clarify biological bases underlying in the development of Hodgkin lymphoma (HL). LMP-1, Epstein-Barr virus (EBV)-derived protein induced JunB and CD30, molecules characteristic for HL cells, during transformation of normal B cells to lymphoblastoid cells. In addition, we found that lymphoblastoid cell line (LCL) already contained stem cell-like population morphologically similar to that had been found in HL. Induction of activated B cell factor-1 (ABF-1), molecule reported as responsible for loss of B-cell phenotype in HL was also induced in LCL.
These results indicated that a part of biological bases, which characterize HL was already induced at early phase of EBV infection to B cells.
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