| Project/Area Number |
25860856
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pediatrics
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| Research Institution | Kyoto University |
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Principal Investigator |
NIWA Akira 京都大学, iPS細胞研究所, 助教 (20546999)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 白血病 / 造血発生 / ＥＳ／ｉＰＳ細胞 / 順遺伝学 / iPS細胞 |
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| Outline of Final Research Achievements |
To elucidate unknown pathogenesis of AML1-ETO (AE) gene in luekemia, we induced hematopoietic cells from PSCs harbouring inducible AE fusion gene cassettes with or without other pathogenic genes such as RTK mutations, and performed in vitro and in vivo assay. First, serial replanting assays in methylcellulose-containing semisolid media as well as liquid culture revealed the strong tendency toward increased colony forming efficacy and suppressed differentiation. In addition to in vitro assays, we next evaluated the in vivo phenotype by transplanting hematopoietic cells into immunodeficient NOG mice. Also in these experiments, we successfully observed the cooperation between AE and RTK mutations for increased engraftment with leukemia-like phenotypes when transplanting immature HSPCs. Those results indicated the successful recapitulation of pathogenic cooperation between AE and RTK mutations in our PSC-derived hematopoietic cells.
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