| Project/Area Number |
25860245
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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 |
Pathological medical chemistry
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| Research Institution | Keio University |
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Principal Investigator |
SUGIHARA Eiji 慶應義塾大学, 医学部, 特任助教 (50464996)
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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 | リンパ腫 / エピジェネィクス / c-Myc / Ezh2 / MEF2B / マウスモデル / エピジェネティクス / 非ホジキンリンパ腫 / バーキットリンパ腫 |
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| Outline of Final Research Achievements |
It has been suggested that deregulation of gene transcription by epigenetic abnormality contributes to tumorigenesis. In this study, we focused on the histone modification-regulated factors Ezh2 and MEF2B whose gene mutations have been often reported, and studied their roles in mature B cell lymphomagenesis. Although mutated Ezh2 enhanced the tri-methylation of histone H3K27, exogenously expression of mutated Ezh2 in germinal center B cells did not induce lymphoma in transplanted mice. MEF2B also showed similar results. On the other hands, c-Myc, frequently overexpressed in lymphoma, could directly induce mature B cell lymphoma. Therefore, mutated histone modification-regulated factors are not direct drivers in lymphomagenesis but probably contribute to the promotion of lymphoma.
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