| Project/Area Number |
23590425
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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 |
Human pathology
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| Research Institution | Osaka University |
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Principal Investigator |
EIICHI Morii 大阪大学, 医学(系)研究科(研究院), 教授 (10283772)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 腫瘍幹細胞 / 制御因子 / 腫瘍 / 子宮内膜癌 / リンパ腫 / 病理学 / マーカー / 発現調節機構 |
|---|
| Research Abstract |
Cancer stem cells (CSCs) are supposed to cause metastasis and recurrence of tumors, because these are restant to various therapies. Here, we analyzed CSCs in various tumors. In Hodgkin lymphoma, small cells with single nucleus were CSCs, which expeled efficiently reactive oxygen species (ROS). In lymphoplasmacytic lymphoma, tumor cells with no expression of B lymphocyte and plasma cell markers were CSCs, because these non-expressing cells yielded B lymphocyte marker-positive and plasma cell marker-positive cells. These non-expressing cells were resistant to anti-cancer drugs and eliminated ROS. Moreover, in endometrioid adenocarcinoma, aldehyde dehydrogenase (ALDH) high cells, which were revealed to be CSCs, were regulated by TGF-beta signal. The inhibition of signal increased ALDH-hi population, and the addition of TGF-beta stimulator reduced ALDH-hi. These results suggested that CSCs were present in various tumors, and their regulation will be necessary for anti-tumor therapies.
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