| Project/Area Number |
21390402
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Yamagata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NEMOTO Kenji 山形大学, 医学部, 教授 (10208291)
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|---|
| Co-Investigator(Renkei-kenkyūsha) |
SUNAYAMA Jun 山形大学, 医学部, 助教 (80466606)
TOMIYAMA Arata 山形大学, 医学部, 助教 (40385810)
TACHIBANA Ken 山形大学, 医学部, 助教 (10400540)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥17,420,000 (Direct Cost: ¥13,400,000、Indirect Cost: ¥4,020,000)
Fiscal Year 2011: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2010: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2009: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
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| Keywords | 脳腫瘍学 / グリオーマ / 幹細胞 / 治療耐性 / 悪性脳腫瘍 / 造腫瘍能 / PI3K / mTOR |
|---|
| Research Abstract |
In this study, we searched for intracellular signals as well as signaling molecules involvedin the maintenance of glioblastoma stem cells and demonstrated critical roles for PI3K/mTOR and MAPK in glioblastoma stem cell maintenance. Significantly, PI3K/mTORand MAPK acted on a common molecule, i.e., the FOXO3 transcription factor, whoseactivity was restrained through phosphorylation by these kinases in glioblastoma stemcells. Our results suggest that FOXO3 as well as these kinases could be rational moleculartargets for stem cell-targeted glioblastoma therapies.
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