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2018 Fiscal Year Final Research Report

Epigenomic analysis with reprogramming technology in lower grade glioma

Research Project

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Project/Area Number 16K10754
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Neurosurgery
Research InstitutionKyoto University

Principal Investigator

Arakawa Yoshiki  京都大学, 医学研究科, 特定講師 (20378649)

Co-Investigator(Kenkyū-buntansha) Thumkeo Dean  京都大学, 医学研究科, 特定准教授 (40372594)
平田 英周  金沢大学, がん進展制御研究所, 准教授 (40761937)
Co-Investigator(Renkei-kenkyūsha) Yamada Yasuhiro  京都大学, iPS細胞研究所, 教授 (70313872)
Research Collaborator Liu Bin  
Fukui Nobuyuki  
Terada Yukinori  
Matsui Yasuzumi  
Makino Yasuhide  
Sumiyoshi Sosuke  
Hattori Etsuko  
Yokogawa Ryuta  
Project Period (FY) 2016-04-01 – 2019-03-31
Keywords低悪性度グリオーマ / ダイレクトリプログラミング / エピゲノム異常 / 分化誘導 / 脳腫瘍 / グリオーマ / エピゲノム / iPS
Outline of Final Research Achievements

Although cell lines and spheroid colony lines were established from glioma surgical specimens containing tumor stem cells, cell lines with IDH1R132H could not be established. Introduction of IDH1R132H into human induced pluripotent stem (iPS) cells and neural stem cells derived from iPS cells impaired those cell proliferation. These results suggest that the IDH1R132H impairs cell survival and proliferation, which is a kind of senescence. Although the culture of cells with IDH1R132H were carried out under conditions using various drugs, difficulty of cell growth was identified. Taken together, we confirmed that it was impossible to establish iPS-derived neural stem cells with IDH1R132H expression.

Free Research Field

脳神経外科

Academic Significance and Societal Importance of the Research Achievements

グリオーマは、未だ根治は困難な疾患である。低悪性度グリオーマの多くは、IDH1/2遺伝子変異が初期の遺伝子異常である。本研究では、IDH1遺伝子変異に伴う腫瘍発生の生物学的意義解明を目指した。その結果、IDH1遺伝子変異伴う細胞老化に似たような現象が神経幹細胞に生じることが、腫瘍発生に関わることを示唆した。

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Published: 2020-03-30  

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