| Project/Area Number |
18K19486
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| Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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| Allocation Type | Multi-year Fund |
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| Review Section |
Medium-sized Section 50:Oncology and related fields
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| Research Institution | Japanese Foundation for Cancer Research |
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Principal Investigator |
TOMIDA Akihiro 公益財団法人がん研究会, がん化学療法センター ゲノム研究部, 部長 (40251483)
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| Project Period (FY) |
2018-06-29 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2020: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2019: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | がん細胞 / 代謝異常 / 相同組換え修復 / 合成致死 |
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| Outline of Final Research Achievements |
In this research project, focusing on homologous recombination (HR) repair deficiency induced by glycolysis inhibition in cancer cells, we proceeded the research to clarify the molecular mechanisms and to establish the POC (Proof Of Concept) as a therapeutic target. Consequently, we succeeded in identifying metabolic inhibitors that induce a cellular phenotype of HR repair deficiency and exhibit a synthetic lethal effect with the anticancer drug cisplatin. Further, by conducting omics and cell biological analyses, we obtained basic information on the mechanisms inducing HR repair failure by metabolic inhibition.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究の学術学的特色は、がん細胞の解糖系阻害によって起こるHR修復不全という独自の知見に基づき、糖代謝を制御し治療効果に結びつけるための新たな戦略を提案しようという点にある。こうした観点から、HR修復不全を誘導できる代謝阻害薬の同定に至った点は、大変意義深いものと考える。また、がんは死亡原因の首位に位置し、有効な治療法の開発は社会的な要請となっているが、本研究はこうした社会的要請に応えるものとして位置づけられるものである。
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