Project/Area Number |
23592128
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Cerebral neurosurgery
|
Research Institution | The University of Tokushima |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
MIZOBUCHI Yoshifumi 徳島大学, 大学院ヘルスバイオサイエンス研究部, 助教 (80547993)
NAGAHIRO Shinji 徳島大学, 大学院ヘルスバイオサイエンス研究部, 教授 (60145315)
MURE Hideo 徳島大学, 病院, 助教 (00624355)
KURASHIKI Yoshitaka 徳島大学, 病院, 特任助教 (10597503)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥130,000 (Direct Cost: ¥100,000、Indirect Cost: ¥30,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
Keywords | 脳腫瘍 / REIC / Wntシグナル / 薬物排出ポンプ / REIC/Dkk-3 / アポトーシス / glioblastoma / Wnt シグナル |
Research Abstract |
Glioblastoma multiform (GBM) remains incurable despite the use of aggressive and multimodal therapies involving tumor resection, chemotherapy and radiation therapy. The cancer stem cell theory postulates that tumors are sustained by a select cell population with self-renewal ability and the capacity to give rise to a heterogeneous mass of tumor cells. Based on the existence of glioma stem cells for glioblastoma, Saya et al. established the new GBM model. Elsewhere we demonstrated that Dickkopf family3 (DKK3) was down-regulated in GBM cells and that its over-expression drastically inhibited their growth via caspase-dependent apoptosis. The aim of our study was 1) to establish this model in our institute and 2) to assess the efficacy of Ad-DKK3 in the GBM mice model and 3) to verify the mechanisms underlying the efficacy of DKK3. We partly verified the mechanisms underlying the efficacy by DKK3 in GBM and submitted our paper to Cancer Letter.
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