| Project/Area Number |
25462036
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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 |
Digestive surgery
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| Research Institution | Kitasato University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 胃癌 / epigenetic / ｐ53 / 新規治療 / p53 / methylation / apotosis / chemotherapy / cancer / PGP9.5 / NMDAR2B / Cyclin A1 |
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| Outline of Final Research Achievements |
In this study, we investigated p53 mutation in relation to such epigenetic alteration in primary gastric cancer. The methylation profiles of the 3 genes (PGP9.5, NMDAR2B, and CCNA1) involved in the p53 pathway were examined in 163 primary gastric cancers. The effect of epigenetic reversion with chemotherapeutic drugs on apoptosis was also assessed. p53 gene mutations were found in 44 primary gastric tumors, and super-high methylation of any of the 3 genes was only found in cases with wild type p53. Higher p53 pathway aberration was found in cases with male gender, intestinal type, and non-infiltrating type. Epigenetic treatment augmented apoptosis by chemotherapeutic drugs, partially through p53 transcription activity. In gastric cancer, p53 relevant and non-relevant pathways exist, and tumors with either pathway type exhibited unique clinical features. Epigenetic treatments were proved to induce apoptosis partially through p53 activation.
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