2019 Fiscal Year Final Research Report
Molecular mechanism of de novo colorectal carcinoma
| Project/Area Number |
17K08691
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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)
岩渕 三哉 新潟大学, 医歯学系, 教授 (70143766)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Keywords | 大腸癌 / de novo癌 / 発生メカニズム / DNA二重鎖切断 / p53 / ミスマッチ修復遺伝子 / 免疫染色 |
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| Outline of Final Research Achievements |
The molecular mechanism involved in the development of de novo colorectal carcinoma (de novo CRC) has not been clarified. In this study, we immunohistochemically investigated 47 cases of pT1 de novo CRC, whether or not p53 gene abnormality, mismatch repair gene abnormality, and DNA damage are involved in their development. As the results, it was suggested that p53 gene abnormality is, and mismatch repair gene abnormality is not involved in de novo CRC development, respectively. Furthermore, DNA damage (double-strand breaks) is more intimately related to their development than other histogenetic pathways of the CRC. It is suggested that the background of the development of de novo CRC may be the colonic microenvironment, which is likely to cause DNA damage.
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| Free Research Field |
人体病理学
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| Academic Significance and Societal Importance of the Research Achievements |
日本人の大腸癌による死亡数は肺癌に次いで多い。大腸癌の中には、腺腫などの前癌病変から発生するものも多く、それらは大腸癌早期発見のターゲット病変となるが、正常大腸から直接発生するde novo癌にはターゲット病変はない。本研究では、de novo癌は前癌病変を介した発癌に比べDNAに多くの傷がついていることがわかった。このことから、大腸内のどのような微小環境が細胞のDNAに傷を付けやすいかが分かれば、de novo癌を早期に発見することが可能になると考えられる。
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