| Project/Area Number |
18K08288
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 53050:Dermatology-related
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| Research Institution | Nippon Medical School (2019-2020)
Akita University (2018) |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | メラノーマ / イノシトールリン脂質 / INPP4B / PTEN / PI3K経路 / 免疫チェックポイント阻害薬 / シグナル伝達 / ノックアウトマウス |
|---|
| Outline of Final Research Achievements |
Intracellular PIP3, one of the inositol phospholipids, is closely related to carcinogenesis. In this study, we used melanoma mice lacking the Inpp4b gene, which was recently found to be involved in PIP3 production, to examine whether the malignancy of melanoma becomes more progressive as the amount of intratumoral PIP3 increases (PIP3 threshold model). The results suggest that Inpp4b heterozygous deleted melanomas are more malignant and resistant to treatment than Inpp4b homozygous deleted melanomas.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究によりPIP3閾値モデルがメラノーマにも一部当てはまることが示唆された。腫瘍内PIP3量の増加は免疫チェックポイント阻害薬に対する感受性を低めることが報告されており、Inpp4bがメラノーマにおいてもPIP3量の増加に関わることを明らかにした本研究は、今後メラノーマの悪性度、治療抵抗性のメカニズムの解明につながる。
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