| Project/Area Number |
24390269
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Research Institute for Clinical Oncology, Saitama Cancer Center (2014)
Chiba Cancer Center (Research Institute) (2012-2013) |
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Principal Investigator |
KAMIJO Takehiko 埼玉県立がんセンター(臨床腫瘍研究所), その他部局等, その他 (90262708)
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| Co-Investigator(Kenkyū-buntansha) |
田尻 達郎 京都府立医科大学, 大学院, 教授 (80304806)
吉田 英生 千葉大学医学系研究科, 研究院, 教授 (60210712)
竹信 尚典 千葉県がんセンター, 研究所, 研究員 (60392247)
春田 雅之 埼玉県立がんセンター, 臨床腫瘍研究所, 研究員 (80392190)
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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 |
¥17,940,000 (Direct Cost: ¥13,800,000、Indirect Cost: ¥4,140,000)
Fiscal Year 2014: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2012: ¥7,670,000 (Direct Cost: ¥5,900,000、Indirect Cost: ¥1,770,000)
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| Keywords | 癌幹細胞 / 腫瘍スフェア / 神経芽腫 / 網羅的解析 / 癌 / 遺伝子 / 小児がん / 小児腫瘍学 / がん幹細胞 |
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| Outline of Final Research Achievements |
We performed screening of molecules which specifically expressed in neuroblastoma sphere and its high expression related to poor prognosis of neuroblastoma patients. Finally, we identified two interesting candidates by the wet/dry experiments; the candidate molecules were co-receptor molecule CXX1 and transcription factor HXX1. Knockdown of co-receptor molecule CXX1 in sphere-forming neuroblastoma cells successfully inhibited sphere formation.
Further, using yeast two-hybrid screening, we identified receptor-type protein tyrosine phosphatase K (PTPRK) as a binding partner of CD133, a cancer stemness-related molecule. Silencing of PTPRK elevated the tyrosine phosphorylation of CD133, while forced expression of PTPRK reduced its phosphorylation level markedly and abrogated CD133-mediated AKT phosphorylation. The tyrosine phosphorylation of CD133, which is dephosphorylated by PTPRK, regulates AKT signaling and plays a critical role in tumorigenesis (ONCOGENE, 2015).
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