| Project/Area Number |
22591163
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Ehime University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
EGUCHI Mariko 愛媛大学, 大学院・医学系研究科, 准教授 (40420781)
ISHII Eichi 愛媛大学, 大学院・医学系研究科, 教授 (20176126)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 小児腫瘍学 / TEL/ETV6 / TEL-AML1 / ES細胞 / 造血細胞分化 / 白血病 |
|---|
| Research Abstract |
To explore the mechanism leading to leukemogenesis by TEL-AML1 fusion gene, mouse ES cells which stably express TEL-AML1 were established, and were differentiated into hematopoietic lineages including B lymphocytes. TEL-AML1-expressing ES cells were capable of differentiating into Flk1-positive mesodermal cells as well as wild-type ES cells, but numbers of produced c-kit+/Sca1+hematopoietic stem cells were significantly reduced compared to control ES cells. Expression of transcriptional factor E2a, which is essential for B lymphocyte differentiation, was retaied in TEL-AML1-expressing ES cells, and immature B lymphocytes could be producedafter 3 to 4 weeks when co-cultured on OP9 stromal cells. On the other hand, TEL-AML1-expressing hematopoietic cells did not confer any growth advantage indicating that at least other genetic abnormalities are necessary for leukemic transformation by TEL-AML1.
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