| Project/Area Number |
18K19480
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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 | Kumamoto University |
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Principal Investigator |
ITO Takaaki 熊本大学, 大学院生命科学研究部(医), 教授 (70168392)
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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 |
¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
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: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 小細胞肺癌 / マウスモデル / オルガノイド / 単離上皮 / オルガノイド発癌 / 神経内分泌分化 / Ascl1 / Rb1 / Notchシグナル / マウス胎仔肺 / 器官培養 / Rb1変異 / p53変異 / Notchシグナル不活化 / GEMM / 胎仔肺 |
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| Outline of Final Research Achievements |
We have established mouse small cell lung cancer (SCLC) model combinding Tp53 KO, Rb1KO and inacitivation of Notch signaling (Hes1 KO) mice, and isolated epithelia obtained from the mouse SCLC model, and cultured them within Matrigel. After about 100 days of cultivation, epithellial proliferative lesions ocurred. After 200days of cultivation, neoplastic cells grew out of the Matrigel with adhesiove or floating pattern. These tumor cells were inoculated in the subcutaneous tissue of the immune-deficinet mice, and histological features of the xenotransplantd tumors were examined. Various histological types of lung cancer including squamous cell carcinoma, adenocarcinoma and small cell carcinoma were detected.
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| Academic Significance and Societal Importance of the Research Achievements |
私達は、Tp53KO, Rb1KO,Notchシグナル不活化による新たな小細胞肺癌マウスモデルを作成し、さらに、このマウスの胎仔肺上皮から、in vitroでの小細胞肺癌発生モデルの開発にも成功した。このことは、この難治性の腫瘍の発生過程を試験管内で再現でき、この腫瘍の発生過程の研究、また、予防、治療、などへと発展できる研究モデルを開発したことになり、学術的にも社会的にも有意義な成果といえる。
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