| Project/Area Number |
15K09479
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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 |
Hematology
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| Research Institution | University of Miyazaki |
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Principal Investigator |
Kubuki Yoko 宮崎大学, 医学部, 講師 (00284836)
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| Co-Investigator(Kenkyū-buntansha) |
北中 明 川崎医科大学, 医学部, 准教授 (70343308)
下田 和哉 宮崎大学, 医学部, 教授 (90311844)
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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 |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | ① 成人T細胞性白血病・リンパ腫 / TET2 / HBZ / 成人T細胞性白血病・リンパ腫 / 遺伝子変異 / 成人Ｔ細胞性白血病・リンパ腫 |
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| Outline of Final Research Achievements |
In this study, analyses were performed, focusing on mutation of TET2, an epigenetic regulator, which is observed in about 10% of ATLL and is expected to be involved in the disease onset and development. Clinical analysis between TET2 mutant patients and TET2 wild-type patients revealed that extranodal lesions were more frequent in the former than the latter. In mouse model analysis, organ infiltration of lymphocytes was more enhanced in HBZ-transgenic/TET2-mutant compound mice, compared to HBZ-transgenic mice that reflect HLTV-1 chronic infection. It seems that TET2 mutation accelerates organ infiltration of ATLL cells, resulting in the disease progression.
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