| Project/Area Number |
25460699
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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 |
Laboratory medicine
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| Research Institution | Juntendo University |
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Principal Investigator |
Sato Eriko 順天堂大学, 医学部, 准教授 (60398675)
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| Co-Investigator(Kenkyū-buntansha) |
KOMATSU Norio 順天堂大学, 医学部, 教授 (50186798)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 慢性骨髄性白血病 / BCR/ABLキメラ遺伝子 / 病態モニタリング / 病態モニタリング技術 / BCR/ABL融合点 / キメラ遺伝子 |
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| Outline of Final Research Achievements |
The aim of this study is to develop a method for monitoring the minimal residual disease in chronic myeloid leukemia (CML). Because of the low expression level of the BCR/ABL mRNAs in CML progenitor cells, conventional monitoring methods targeting BCR/ABL mRNAs cannot predict the relapse of CML. Here, we have developed the method to identify the BCR/ABL breakpoint in genomic DNAs. BCR/ABL breakpoint in genomic DNAs is expected to be a surrogate marker of minimal CML cells because the copy number of DNAs correspond to the number of cells. We demonstrated the BCR/ABL breakpoints of of K562, KCL-22, and TCC-S cells can be detected using the method. Furthermore, we were able to construct the highly sensitive monitoring method targeting the identified breakpoint in two of the three cell lines (K562 and KCL-22). Although the method should be brushed up for the practical use, the method has a potential to detect a single CML cell in patients with CML.
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