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An attempt to answer the cardinal question --- why do cancer cells have such a sweet tooth? --- through glioma stem cell research

Research Project

Project/Area Number 15K15522
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field Neurosurgery
Research InstitutionYamagata University

Principal Investigator

KITANAKA Chifumi  山形大学, 医学部, 教授 (70260320)

Co-Investigator(Renkei-kenkyūsha) OKADA MASASHI  山形大学, 医学部, 講師 (70512614)
Project Period (FY) 2015-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Keywordsglioma-initiating cell / 神経膠芽腫
Outline of Final Research Achievements

Glucose metabolism is often increased in human cancers, the significance of which for cancer cells remains mostly unclear. In this project, we conducted experiments to test the working hypothesis that glucose metabolism contributes to the maintenance of glioma stem cells through the modulation of intracellular ROS levels as well as to investigate the mechanism underlying the increase in intracellular ROS levels caused by impaired glucose metabolism via GLUT1 inhibition. While the results of this study supported the idea that increase in intracellular ROS levels leads to loss of stem cell properties, the molecular mechanism of ROS increase following GLUT1 inhibition remains to be shown.

Report

(3 results)
  • 2016 Annual Research Report   Final Research Report ( PDF )
  • 2015 Research-status Report
  • Research Products

    (4 results)

All 2016 2015

All Journal Article (1 results) (of which Peer Reviewed: 1 results,  Acknowledgement Compliant: 1 results) Presentation (3 results) (of which Invited: 2 results)

  • [Journal Article] GSKJ4, a selective Jumonji H3K27 demethylase inhibitor, effectively targets ovarian cancer stem cells2015

    • Author(s)
      Sakaki et al.
    • Journal Title

      Anticancer Research

      Volume: 15 Pages: 6607-6614

    • Related Report
      2015 Research-status Report
    • Peer Reviewed / Acknowledgement Compliant
  • [Presentation] 促進性グルコース輸送体GLUT1阻害は癌幹細胞の自己複製能と腫瘍形成能を抑制する.2016

    • Author(s)
      岡田雅司, 鈴木修平, 清野学, 武田弘幸, 北中千史
    • Organizer
      第75回日本癌学会学術総会
    • Place of Presentation
      パシフィコ横浜(横浜)
    • Related Report
      2016 Annual Research Report
  • [Presentation] グルコース代謝の抑制はがん幹細胞の幹細胞性維持および腫瘍創始能を抑制する.2016

    • Author(s)
      2) 岡田雅司, 北中千史
    • Organizer
      第59回放射線影響学会
    • Place of Presentation
      JMSアステールプラザ(広島)
    • Related Report
      2016 Annual Research Report
    • Invited
  • [Presentation] グリオーマ、固形がん幹細胞を標的とする治療法開発を目指したがん幹細胞研究2015

    • Author(s)
      北中 千史
    • Organizer
      第74回癌学会学術総会
    • Place of Presentation
      名古屋国際会議場(愛知県名古屋市)
    • Year and Date
      2015-10-08
    • Related Report
      2015 Research-status Report
    • Invited

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Published: 2015-04-16   Modified: 2018-03-22  

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