| Project/Area Number |
25462272
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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 |
Neurosurgery
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| Research Institution | Kumamoto University |
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Principal Investigator |
Shinojima Naoki 熊本大学, 医学部附属病院, 寄附講座教員 (50648269)
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| Co-Investigator(Kenkyū-buntansha) |
倉津 純一 熊本大学, 大学院生命科学研究部(医), 教授 (20145296)
中村 英夫 熊本大学, 医学部附属病院, 講師 (30359963)
秀 拓一郎 熊本大学, 医学部附属病院, 診療講師 (40421820)
矢野 茂敏 熊本大学, 大学院生命科学研究部(医), 准教授 (60332871)
牧野 敬史 熊本大学, 医学部附属病院, 講師 (90381011)
黒田 順一郎 熊本大学, 大学院生命科学研究部(医), 助教 (90536731)
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| Research Collaborator |
Lang Frederick F. Department of Neurosurgery, The University of Texas M. D. Anderson Cancer Center, Professor
Tasaki Masayoshi 熊本大学, 大学院生命科学研究部保健学系構造機能解析学, 助教
Ando Yukio 熊本大学, 大学院生命科学研究部・神経内科学, 教授
Ichimura Koichi 国立がん研究センター研究所, 脳腫瘍連携研究分野, 分野長
Mikami Yoshiki 熊本大学, 医学部附属病院・病理診断科, 教授
Takakura Nobuyuki 大阪大学, 微生物病研究所・情報伝達分野, 教授
Era Takumi 熊本大学, 発生医学研究所幹細胞部門・幹細胞誘導分野, 教授
Yamada Kazumichi 熊本大学, 医学部附属病院・脳神経外科・機能神経外科先端医療寄付講座, 特任教授
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | グリオーマ幹細胞 / 腫瘍関連間質細胞 / CD44 / 再発・再増大 / Niches / 悪性グリオーマ / 膠芽腫 / 放射線壊死 / Niche / 再発 / ｸﾞﾘｵｰﾏ幹細胞(GICs) / 骨髄由来間葉系幹細胞 / 腫瘍抑制性microRNA |
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| Outline of Final Research Achievements |
Glioblastoma, a representative of malignant gliomas, is a lethal tumor with a median survival time of about 15 months. As one of the mechanisms of the resistance to the treatment, it is suggested that glioma initiating cells (GICs) exist in the quiescent state by exiting from growth and division cycles and remaining in G0 state. Radiation and chemotherapy are able to kill regular tumor cells existing in growth and division cycles, but not GICs existing in the quiescent state, resulting in survival of GICs. Thus GICs enter into the growth and division cycle from G0 state by some cues, proliferate, and as a result they will recur. In this study, we found that CD44+ cancer associated stromal cells may be involved in the regulation of GICs' proliferation as the niches. It has been suggested that control of the CD44+ stromal cells leads to the control of recurrence.
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