Strategy of anti-cancer therapy for gastrointestinal cancers targeting non-oncogenic addiction
| Project/Area Number |
15K10126
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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 | National Hospital Organization, Beppu Medical Center (2017)
National Hospital Organization, Kyushu Medical Center (Clinical Institute) (2015-2016) |
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Principal Investigator |
Egashira Akinori 独立行政法人国立病院機構別府医療センター(臨床研究部), 臨床研究部, その他 (00419524)
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| Co-Investigator(Kenkyū-buntansha) |
藤 也寸志 独立行政法人国立病院機構(九州がんセンター臨床研究センター), その他部局等, 院長 (20217459)
森田 勝 独立行政法人国立病院機構(九州がんセンター臨床研究センター), その他部局等, その他 (30294937)
山本 学 国際医療福祉大学, 福岡看護学部, 教授 (30380405)
南 一仁 独立行政法人国立病院機構(九州がんセンター臨床研究センター), その他部局等, 消化器外科医師 (50522851)
沖 英次 九州大学, 大学病院, 助教 (70380392)
佐伯 浩司 九州大学, 大学病院, 助教 (80325448)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | DNA修復機構 / p53 / 食道癌 / 神経内分泌癌 / c-kit / DNA修復 / 消化器癌 / 術前化学療法 |
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| Outline of Final Research Achievements |
Since the DNA mismatch repair could be associated with the hereditary non-polyposis colorectal, an inherited disorder of MUTYH DNA glycosylase, which removes mutagenic oxidized base from DNA, has been reported in MUTYH-associated polyposis, the connection between impairment of DNA repair function and gastrointestinal cancer is apparent. Esophagus always suffer from exposure to endogenous and exogenous mutagens, such as alcohol and cigarette smoking, the role of DNA repair pathway in preventing carcinogenesis might be quite important.
From the analysis of neuroendocrine carcinoma of the esophagus, the relationship between abnormality of p53, which is the key molecular of DNA repair, and the disruption of c-kit protein-related signal transmission pathway is presented. These results provide new insight into the understanding of the mechanism of carcinogenesis, and which in turn might be connecting the innovative treatment.
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Report
(4 results)
Research Products
(16 results)
