2000 Fiscal Year Final Research Report Summary
Genetic changes in flat type and polypoid type colo-rectal cancer in early stages
| Project/Area Number |
10671213
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Jichi Medical School |
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Principal Investigator |
KONISHI Fumio Jichi Medical School, Department of Surgery, Professor, 医学部, 教授 (20142242)
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| Co-Investigator(Kenkyū-buntansha) |
OKADA Masaki Jichi Medical School, Department of Surgery, Lecturer, 医学部, 講師 (40254924)
SATOH Tomoyuki Jichi Medical School, Department of Surgery, Assistant, 医学部, 助手 (50225976)
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| Project Period (FY) |
1998 – 2000
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| Keywords | flat type colorectal cancer / polypoid type colorectal cancer / microsatellite instability / apoptosis / p53 |
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| Research Abstract |
The present research was conducted to clarify the genetic changes in flat type early colorectal carcinomas and polypoid type early colorectal carcinomas. The percentage of Ki-ras point mutation was significatly smaller in flat type than in polypoid type lesions. In the right side of the colon, the percentage of microsatellite instability was higher in flat type than in polypoid type carcinomas in early stages. In more advanced carcinomas of the right side of the colon, the MSI positive lesions showed higher percentage of Ki-ras mutation. Therefore, in the right side of the colon, flat type carcinomas in early stages can be considered to be a candidate for the MSI positive advanced carcinoma. However, in the left side of the colon and rectum, such results were not demonstrated. In flat-type carcinoma apoptotic index (Tunnel Index) in the p53 protein overexpression group was significantly smaller than that in the p53 protein-negative group (P < 0.05). The Ki-67 labeling index/Tunnel ratio in the p53 protein overexpression group was significantly higher than that in the p53 protein-netative tour (P < 0.05). In rolvroid-type carcinoma, no significant difference in the ratio was shown between the p53 protein overexpression group and p53 protein-negative group. Therefore, p53-dependent apoptosis may contribute to the development of flat-type early colorectal carcinoma. In summery, it was considered that there would be different genetic changes involved in the two different types of colorectal carcinomas in early changes.
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