• Search Research Projects
  • Search Researchers
  • How to Use
  1. Back to previous page

Development of new therapeutic strategies to prevent stem cell formation of glioblastoma by epigenetics control

Research Project

Project/Area Number 16K10771
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Neurosurgery
Research InstitutionTokyo Women's Medical University

Principal Investigator

Nitta Masayuki  東京女子医科大学, 医学部, 助教 (70588269)

Co-Investigator(Kenkyū-buntansha) 丸山 隆志  東京女子医科大学, 医学部, 講師 (40301543)
赤川 浩之  東京女子医科大学, 医学部, 准教授 (60398807)
増井 憲太  東京女子医科大学, 医学部, 助教 (60747682)
安田 崇之  東京女子医科大学, 医学部, 助教 (70725366)
都築 俊介  東京女子医科大学, 医学部, 助教 (90746794)
Research Collaborator Muragaki Yoshihiro  
Project Period (FY) 2016-04-01 – 2019-03-31
Project Status Completed (Fiscal Year 2018)
Budget Amount *help
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Keywordsglioblastoma / stem cell / cMyc / anti tumor effect / 膠芽腫 / エピジェネティクス / myc / 腫瘍幹細胞 / 再発 / 脳腫瘍学
Outline of Final Research Achievements

The following results were obtained as a result of this research.
In glioblastoma, the expression of stem cell markers such as cMyc and Sox2 was higher at the time of relapse than at the time of relapse. This suggested that tumor recurrence is associated with stem cell formation of tumor cells. Next, when cultured cells from tumor tissue were established, and a drug that suppresses cMyc expression was administered using a cell line with high cMyc expression, and a DNA-damaging anticancer agent, it showed an antitumor effect against single drug administration. These findings form the basis for a treatment that suppresses stem cell formation in glioblastoma

Academic Significance and Societal Importance of the Research Achievements

致死性が高く、有効な治療法が存在しない膠芽腫は平均生存期間が2年に満たない非常に悪性度の高い腫瘍で、腫瘍の中に存在する幹細胞が治療抵抗性の原因の一つと考えられている。今回の成果は、腫瘍の幹細胞化を抑制することを用いた新たな治療法の開発の基礎となったと考えられる

Report

(4 results)
  • 2018 Annual Research Report   Final Research Report ( PDF )
  • 2017 Research-status Report
  • 2016 Research-status Report
  • Research Products

    (3 results)

All 2019 2018

All Journal Article (3 results) (of which Peer Reviewed: 2 results,  Open Access: 1 results)

  • [Journal Article] 特別寄稿 脳神経外科コントロバーシー2019 (7)グレード2神経膠腫に対する治療方針-手術・放射線治療・化学療法2019

    • Author(s)
      新田 雅之、村垣 善浩
    • Journal Title

      Neurological Surgery 脳神経外科

      Volume: 47 Issue: 2 Pages: 147-158

    • DOI

      10.11477/mf.1436203913

    • ISSN
      0301-2603, 1882-1251
    • Year and Date
      2019-02-10
    • Related Report
      2018 Annual Research Report
  • [Journal Article] A surgical strategy for lower grade gliomas using intraoperative molecular diagnosis2018

    • Author(s)
      Koriyama Shunichi、Nitta Masayuki、Kobayashi Tatsuya、Muragaki Yoshihiro、Suzuki Akane、Maruyama Takashi、Komori Takashi、Masui Kenta、Saito Taiichi、Yasuda Takayuki、Hosono Junji、Okamoto Saori、Shioyama Takahiro、Yamatani Hiroaki、Kawamata Takakazu
    • Journal Title

      Brain Tumor Pathology

      Volume: 35 Issue: 3 Pages: 159-167

    • DOI

      10.1007/s10014-018-0324-1

    • Related Report
      2018 Annual Research Report
    • Peer Reviewed
  • [Journal Article] Elevated TERT Expression in TERT-Wildtype Adult Diffuse Gliomas: Histological Evaluation with a Novel TERT-Specific Antibody.2018

    • Author(s)
      Masui K, Komori T, Kato Y, Masutomi K, Ichimura K, Ogasawara S, Kaneko MK, Oki H, Suzuki H, Nitta M, Maruyama T, Muragaki Y, Kawamata T, Sawada T, and Shibata N
    • Journal Title

      BioMed Research International

      Volume: - Pages: 95-99

    • DOI

      10.1155/2018/7945845

    • Related Report
      2018 Annual Research Report
    • Peer Reviewed / Open Access

URL: 

Published: 2016-04-21   Modified: 2020-03-30  

Information User Guide FAQ News Terms of Use Attribution of KAKENHI

Powered by NII kakenhi