| Project/Area Number |
26460415
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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 |
Human pathology
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| Research Institution | Niigata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
若井 俊文 新潟大学, 医歯学系, 教授 (50372470)
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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 |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 大腸癌の発生 / 腺腫の癌化 / 鋸歯状病変 / 炎症性発癌 / DNA二重鎖切断 / DNA損傷修復応答 / 蛍光二重免疫染色 / 大腸鋸歯状病変 / SSA/P / γH2AX / 免疫組織化学 |
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| Outline of Final Research Achievements |
Colorectal carcinogenesis occurs through various pathways; ①de novo cancerization (carcinogenesis in normal mucosa), ②adenoma-carcinoma sequence, ③cancerization from hyperplastic polyp or SSA/P, ④inflammatory carcinogenesis occurs in inflammatory mucosa such as ulcerative colitis. This study investigated whether or not DNA damage and DNA damage response play a role in these carcinogenetic pathways. As the result, it was speculated that accumulation of DNA damage play a role in cancerization in non-neoplastic inflammatory mucosa in pathway-④, and in precancerous lesions in pathway-②③. DNA damage response failure may play a role in development of invasive carcinoma.
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