| Project/Area Number |
22300344
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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 |
Clinical oncology
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| Research Institution | Aichi Cancer Center Research Institute |
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Principal Investigator |
KONDO Yutaka 愛知県がんセンター(研究所), ゲノム制御研究部, 部長 (00419897)
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| Co-Investigator(Renkei-kenkyūsha) |
TOYOTA Minoru 札幌医科大学, 医学部生化学, 教授 (70270676)
NATSUME Atsushi 名古屋大学, 大学院脳神経外科学, 准教授 (30362255)
UESUGI Motonari 京都大学, 物質-細胞統合システム拠点, 教授 (10402926)
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| Project Period (FY) |
2010-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥15,860,000 (Direct Cost: ¥12,200,000、Indirect Cost: ¥3,660,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2011: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2010: ¥9,360,000 (Direct Cost: ¥7,200,000、Indirect Cost: ¥2,160,000)
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| Keywords | 分子標的治療 / がん幹細胞 / ポリコーム / グリオブラストーマ / エピジェネティクス / ポリコーム複合体 / ヒストン修飾 / 脳腫瘍 |
|---|
| Research Abstract |
Glioblastoma is the most common and deadly primary brain tumor, which is characterized by intratumoral and intertumoral heterogeneity with histologically different types of cells. Such multiple distinct subpopulations of cancer cells within tumors link to the existence of cells that survive surgery and chemotherapy to form recurrent lesions that are resistant to further treatments. Elucidating the molecular mechanisms underlying tissue heterogeneity of glioblastoma is a fundamental requirement for the development of effective treatments for this dreadful disease. We revealed that H3K27me3 mediated by EZH2/PRC2, which controls tumor cell plasticity, may provide a target to restrict the functional heterogeneity in tumors, a core challenge to all cancer cell-centric drugs given the huge reservoir of resistance mechanisms which such heterogeneity confers. In order to identify the EZH2/PRC2 inhibitor, we developed a high-throughput screening for chemicals and assayed 15,000 compounds.
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