| Project/Area Number |
24590377
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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 | Nagoya University |
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Principal Investigator |
KISHIDA Satoshi 名古屋大学, 医学(系)研究科(研究院), 助教 (20402563)
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| Co-Investigator(Kenkyū-buntansha) |
KADOMATSU Kenji 名古屋大学, 大学院医学系研究科, 教授 (80204519)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 神経芽腫 / モデルマウス / 自然退縮 / トランスジェニックマウス / 神経堤 / 神経芽種 / 次世代シーケンサー / がん幹細胞 |
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| Outline of Final Research Achievements |
In this research, we tried to identify the genes involved in the tumorigenesis of neuroblastoma, one of the malignant pediatric solid tumors. Based on our comprehensive data acquired from MYCN transgenic (Tg) mice, we identified two genes, NeuroD1 and H1FX. Both were highly expressed in the early lesions of MYCN Tg mice. We showed that NeuroD1 directly induced the transcription of ALK, an important predisposeition gene in neuroblastoma. NeuroD1-ALK axis promotes the proliferation of neuroblastoma cells. On the other hand, H1FX seems to be involved in the early development of sympathetic neurons. H1FX was highly and specifically expressed in totally undifferentiated neuroblast in vivo, and disappeared after differentiation. Interestingly, the expression of H1FX in patients was closely correlated with that of Midkine, a growth factor involved in neuroblastoma tumorigenesis. H1FX could be a target of midkine signaling.
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