| Project/Area Number |
16K10167
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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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| Research Field |
Dermatology
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| Research Institution | University of the Ryukyus |
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Principal Investigator |
Kinjo Takao 琉球大学, 医学部, 教授 (30284962)
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| Co-Investigator(Kenkyū-buntansha) |
常木 雅之 新潟大学, 歯学部, 医員 (40714944)
高橋 健造 琉球大学, 医学(系)研究科(研究院), 教授 (80291425)
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| Research Collaborator |
TANABE Yasuka 琉球大学, 医学部, 技術専門職員 (80437996)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | カポジ肉腫 / HHV-8 / K1遺伝子 / 形質転換能 / 古典型 / 自然消退 / 臨床像 / KSHV / 遺伝子 / 病理学 |
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| Outline of Final Research Achievements |
Kaposi’s sarcoma (KS) is caused by humanherpesvirus-8 (HHV-8) and subdivided four types based on clinical presentations. Among these subtypes, clinical presentations of classic type KS are milder than those of AIDS-related KS. In particular, the lesions of classic type KS are limited to the skin and sometimes show spontaneous regression. HHV-8 encodes K1 gene which is involved in KS oncogenesis. Because we found amino acid sequence variations of K1 gene between classic type KS and AIDS-related KS, we hypothesized that the transformation activities of K1 gene between classic KS and AIDS-related KS are associated with their clinical presentations. In this research, we revealed that transformation activity of classic type KS is weaker than that of AIDS-related KS suggesting possible association with spontaneous regression seen in classic type KS. The mechanism of spontaneous regression of classic KS may provide new therapeutic strategy against cancer.
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| Academic Significance and Societal Importance of the Research Achievements |
これまでAIDS関連型KSと古典型KSの臨床症状が何故異なるか明らかではなかった。HHV-8のK1遺伝子は腫瘍発生に関わる事が知られていたが、本研究では古典型KS由来K1遺伝子はAIDS関連型KS由来K1遺伝子より形質転換能が弱い事を明らかにした。HHV-8のK1遺伝子の機能が臨床症状に関連する事を初めて報告した。古典型KSの自然消退のメカニズムの解明は、将来的に癌の自然消退を誘導する治療法を開発する上で基盤となると考えられる。
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