| Project/Area Number |
16K20232
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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 |
Otorhinolaryngology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
Kobayashi Kenya 東京大学, 医学部附属病院, 登録研究医 (80648311)
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| Research Collaborator |
Ando Mizuo
Kondo Kenzi
Yoshida Masahumi
Saito Yuki
Omura Go
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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 |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 腺様嚢胞癌 / MYB-NFIB癒合遺伝子 / 免疫逃避機構 / PDL1 / 癒合遺伝子 / PD-L1 / NTRK / 神経周囲浸潤 / 神経栄養因子 / PD-Ｌ1 |
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| Outline of Final Research Achievements |
In this study, we analyzed molecular biological features of 37 adenoid cystic carcinoma tumor specimens. PD-L1 expression analysis by immunostaining revealed 21% cases are overexpressed PD-L1(positive cell >10%). PD-L1 overexpression was significantly associated with poor local control rate. In FISH analysis, MYB-NFIB fusion gene were detected in 51% cases. To detected novel NTRK (coding Trk recepter) fusion gene, we performed RNA sequencing for Nerve Growth factor/TrkA receptor overexpress tumor, however there were no detection of novel fusion gene. Gene expression analysis of RNA sequencing, high frequent mutation was SP1, CEP57, DST, FGFR2, KANK1, EPCAM, NOTCH1.
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| Academic Significance and Societal Importance of the Research Achievements |
腺様嚢胞癌は外科治療以外に有効治療がない難治性腫瘍である。その理由として、希少癌であること、神経周囲浸潤・遠隔転移を来しやすいこと、有効な薬剤がないことなどが上げられており、腫瘍の分子生物学的特徴の解明は急務である。本研究では、腺様嚢胞癌の免疫逃避機構の関連、予後との相関を明らかにし、発癌に関与する融合遺伝子も検討した。さらに、変異頻度が高い遺伝子を同定したことで、治療開発に役立つ可能性がある。
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