| Project/Area Number |
16K20968
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Veterinary medical science
Integrative animal science
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| Research Institution | The University of Tokyo |
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Principal Investigator |
SAEKI Kohei 東京大学, 大学院農学生命科学研究科(農学部), 特任助教 (30769005)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | BRAF / COX2 / PGE2 / がん微小環境 / BRAF遺伝子変異 / MAPK / 犬膀胱移行上皮癌 / 移行上皮癌 / プロスタグランジン |
|---|
| Outline of Final Research Achievements |
In this study, significance of BRAF gene mutation on both of cell proliferation/survival and tumor microenvironment/inflammation was evaluated using canine transitional cell carcinoma (cTCC). As a result, impact of activation of RAF/MEK/ERK pathway, subsequent to BRAF gene mutation, on cTCC cell proliferation was not significant or dispensable due to presence of other possible bypass pathways. On the other hand, activation of BRAF pathway was strongly associated with COX expression and PGE2 production in the tumor cells. In evaluation of cTCC clinical samples, it was revealed that BRAF-mutant cTCC tissues tended to have higher COX2 immunostaining score. In addition, it was suggested that inflammatory environment induced by COX-2 was not identical between wild-type cTCC and BRAF mutant.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究ではイヌの移行上皮癌をもちいてがん遺伝子に起こった変異とそれにより直接活性化された細胞内シグナルが、がん微小環境の炎症状態を誘導している可能性を明らかにした。癌に対する抗炎症治療を実施する上で新たな概念を立証した重要な一歩である。
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