| Project/Area Number |
23591627
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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 |
Dermatology
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| Research Institution | Takasaki University of Health and Welfare |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
OHTSUKI Mamitaro 自治医科大学, 医学部, 教授 (90185330)
SATO Atsuko 自治医科大学, 医学部, 助教 (50382916)
SAITO Katsuyo 高崎健康福祉大学, 薬学部, 助手 (90455288)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | がん / シグナル伝達 / 発現制御 / 治療感受性 / 生体内イメージング / エピジェネティック修飾 / メラノーマ / 薬剤反応性 |
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| Research Abstract |
BRAF (V600E) is the common oncogenic driver mutation in 60-70% of melanoma patients. Melanoma cells that have BRAF (V600E) mutation accumulated aberrant gene suppression through the histone-chromatin modification, and subsequently the aberrancy was well correlated with metastatic potentials of examined melanoma cells. The histone deacetylase inhibitor (HDACi) is a potent agent to improve the aberrantly deacetylated-histones. Some of HDACi were able to improve levels of deacetylated-histones and sensitized melanoma cells to the therapeutic cell death partially. Unfortunately the effects of HDACi did not always appear sufficient for BRAF (V600E)-positive melanoma cells. Thus, it is necessary to think the possibility that BRAF (V600E)-mediated constitutive activation may maintain the abnormal histone methylation, and that particular gene amplification accompanied with melanoma development may be involved in the therapeutic resistance.
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