| Project/Area Number |
26461575
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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 |
Pediatrics
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| Research Institution | Shinshu University |
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Principal Investigator |
SAKASHITA Kazuo 信州大学, 医学部附属病院, 特任研究員 (10345746)
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| Co-Investigator(Kenkyū-buntansha) |
小池 健一 信州大学, 医学部, 特任教授 (40143979)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 若年性骨髄単球性白血病 / 白血病幹細胞 / PCDH17 / 白血病性幹細胞 / 若年性骨髄単球白血病 / 幹細胞 |
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| Outline of Final Research Achievements |
Juvenile myelomonocytic leukemia (JMML) is a rare myelodyasplastic/myeloproliferative disorder that occurs during infancy and early childhood. Clonogenic JMML progenitors cannot be maintained in culture because they differentiate and the leukemic clone is lost within a few weeks. Here, we demonstrated that AGM-S3 in combination with hematopoietic growth factors expand CD34+CD38－ cells in patients with JMML showing PTPN11, NRAS, or KRAS mutation in the fetal bovine serum-containing culture.
From genome-wide DNA methylation analysis, we demonstrated that there was a significant correlation between methylation status of PCDH17 and event-free survival or overall survival in ALL. PCDH17 methylation at onset may be related to poor prognosis, and a new biomarker to predict relapse in ALL. PCDH17 gene may function as a tumor suppressor gene in leukemic cells. Now we examine the rule of PCDH17 gene in JMML.
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