Role of the tumor microenvironment on radiation-induced carcinogenesis
Project/Area Number |
17K19944
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Research Category |
Grant-in-Aid for Challenging Research (Exploratory)
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Allocation Type | Multi-year Fund |
Research Field |
Health science and related fields
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Research Institution | National Institute of Public Health |
Principal Investigator |
Shimura Tsutomu 国立保健医療科学院, その他部局等, 上席主任研究官 (40463799)
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Project Period (FY) |
2017-06-30 – 2020-03-31
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Project Status |
Completed (Fiscal Year 2019)
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Budget Amount *help |
¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2018: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2017: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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Keywords | 放射線発がん / がんの微小環境 / ミトコンドリア / 活性酸素 / がん関連線維芽細胞 / 酸化ストレス / 微小環境 / ROS |
Outline of Final Research Achievements |
Cancer-associated fibroblasts (CAFs) are an activated from of fibroblasts in tumor tissues. CAF release paracrine factors that promote tumor growth and cancer cell aggressiveness. We investigated the association between oxidative stress and the formation of tumor microenvironments during the development of radiation-related tumors. Reactive Oxygen Species (ROS) play a pivotal role in the process of fibroblasts activation in normal tissue injury. Recovery of damaged cells from radiation is essential for CAF clearance, which restores stromal cell dormancy and prevents tumor microenvironment formation. However, remaining ROS maintained CAF persistence which led to facilitated tumor microenvironment formation. Alterations in stromal cells can contribute to radiation-related tumors. Radiation affects malignant cancer cells directly and indirectly via the tumor stroma.
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Academic Significance and Societal Importance of the Research Achievements |
放射線被ばくによって将来がんになる不安や子孫への遺伝的影響への懸念など被ばくによる精神的ストレスが原因となる二次的な健康影響が問題となっている。放射線による健康影響について、継続して適切な情報を発信することが重要である。本研究の成果は、福島事故後に問題となっている低線量放射線発がんの機序解明の一端となり得るものである。我々は、放射線発がんには、単にがん細胞の遺伝子変異の蓄積だけでなく、がん微小環境の形成が重要であると考える。本申請研究の成果により、放射線発がんリスク評価の根拠となる科学的知見の蓄積が期待される。
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Report
(4 results)
Research Products
(17 results)
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[Journal Article] Overexpression of Rev1 promotes the development of carcinogen-induced intestinal adenomas via accumulation of point mutation and suppression of apoptosis proportionally to the Rev1 expression level.2017
Author(s)
Sasatani M, Xi Y, Kajimura J, Kawamura T, Piao J, Masuda Y, Honda H, Kubo K, Mikamoto T, Watanabe H, Xu Y, Kawai H, Shimura T, Noda A, Hamasaki K, Kusunoki Y, Zaharieva EK, Kamiya K.
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Journal Title
Carcinogenesis.
Volume: 38(5)
Issue: 5
Pages: 570-578
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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