| Project/Area Number |
24890046
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Hematology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
KATAOKA Keisuke 東京大学, 医学部附属病院, 特任助教 (90631383)
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| Project Period (FY) |
2012 – 2013
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 白血病幹細胞 / 急性骨髄性白血病 / p53 / JAK2 / 赤白血病 |
|---|
| Research Abstract |
We retrovirally transduced JAK2V617F into bone marrow cells from p53 wild-type and knockout mice and transplanted them into irradiated recipients. As previously shown, JAK2V617F expression in wild-type hematopoietic cells causes polycythemia vera (PV). In contrast, in the absence of p53, recipients developed fatal leukemia after the preceding PV phase, characterized by expansion of dysplastic erythroid progenitors. These leukemic cells are serially transplantable. Both primitive leukemia cells and erythroid progenitors possess leukemia-initiating capacity, whereas myeloid populations cannot recapitulate the disease.
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