| Project/Area Number |
26293298
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Chiba University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
井ノ上 逸朗 国立遺伝学研究所, 総合遺伝研究系, 教授 (00192500)
阿久津 泰典 千葉大学, 医学(系)研究科(研究院), 講師 (00375677)
村上 健太郎 千葉大学, 医学部附属病院, 助教 (40436382)
田村 裕 千葉大学, 医学(系)研究科(研究院), 准教授 (50263174)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥15,990,000 (Direct Cost: ¥12,300,000、Indirect Cost: ¥3,690,000)
Fiscal Year 2016: ¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2015: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2014: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
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| Keywords | 食道癌 / ゲノム / エピゲノム / 分子治療 / 外科 / 癌 / 遺伝子 / トランスレーショナルリサーチ / 発癌制御 / 全ゲノムシーケンス / がん抑制遺伝子 / 遺伝子変異 / 発現制御 |
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| Outline of Final Research Achievements |
Analysis of allele specific expression in esophageal squamous cell carcinoma with combination of exome sequencing and mRNA Sequencing. Exome sequenceing analysis of 25 ESCC cases identified TP53 and ZNF750 as significantly mutated genes. Each gene was analyzed in detail with combination of DNA sequencing data and RNA sequencing. The expression level of TP53 with splicing site mutations, stopgain mutations, and indels were decreased significantly, which was seemed to cause dysfanction of p53 protein. Although expression of TP53 with nonsynchronous mutation was maintained, frequencies of nonsynchronous mutation allele in RNA were increased than those in DNA, which possibly cause dysfanction of its product. Comparing between normal and tumor tissues, expression of VNF750 were decreased, which ZNF750 expression of 2 cases with nonsynchronous mutations were maintained.
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