| Project/Area Number |
17K08679
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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 |
Pathological medical chemistry
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| Research Institution | Kindai University |
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Principal Investigator |
UEDA Takeshi 近畿大学, 医学部, 准教授 (60585149)
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| Co-Investigator(Kenkyū-buntansha) |
金井 昭教 広島大学, 原爆放射線医科学研究所, 助教 (60549567)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | エピジェネティクス / 遺伝子発現制御 / 造血器腫瘍 / 癌 / 遺伝子 / 発現制御 |
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| Outline of Final Research Achievements |
Lysine demethylase 4B (KDM4B) acts as an epigenetic regulator that belongs to the KDM4 histone demethylase family comprising KDM4A－KDM4D. In this study, we found that KDM4B was highly expressed in cases with acute myeloid leukemia (AML) associated with chromosomal translocation 8;21 [t(8;21)], and investigated the role of this molecule in the disease pathogenesis of AML using human cell lines and a mouse model. As a result, KDM4B was shown to epigenetically promote AML cooperatively with the t(8;21)-fusion gene.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究課題では、ヒストン脱メチル化酵素KDM4Bが特定の染色体異常を有するAMLで発現上昇を認めることに着目し、本因子がクロマチンの構造変化を介して、AMLの病態を促進させることを示した。本研究により、AMLの病態に促進的に働くエピゲノム制御機構の一端が明らかとなった。
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