| Project/Area Number |
24591379
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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 |
Hematology
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| Research Institution | Gunma University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
HANDA Hiroshi 医学部附属病院, 講師 (90282409)
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| Co-Investigator(Renkei-kenkyūsha) |
YAMANE Arito , 大学院医学系研究科, 講師 (10420192)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2013: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2012: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
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| Keywords | ゲノム不安定性 / 多発性骨髄腫 / BCL6 / DNA損傷修復 / AID |
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| Outline of Final Research Achievements |
Multiple myeloma (MM) is plasma cell neoplasm, which is a tumor of terminally differenced B cell. Though genomic instability is considered as one of the underling mechanisms of the tumor progression, its molecular mechanisms remains to be elucidated. AID and BCL6 has been reported to play a pivotal role in B cell tumors but its role in MM has not been studied. In this study, we showed an abundant expression level of BCL6 in myeloma cells but not AID. We evaluated the role of BCL6 in DNA damage responses. BCL6 negatively regulated the expression of ATM and therefore inhibited the formation of gamma H2AX upon X irradiation, which can lead to genomic instability in the myeloma cell treated with anti cancer drugs and irradiation.
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