Role of premalignant lesion and its significance in the promotion/progssion stage of colon carcinogenesis in Apc min mice.
| Project/Area Number |
15390124
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Experimental pathology
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| Research Institution | Gifu University |
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Principal Investigator |
MORI Hideki Gifu University, Graduate School of Medicine, Department of Tumor Pathology, Professor, 大学院・医学研究科, 教授 (70021433)
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| Co-Investigator(Kenkyū-buntansha) |
YAMADA Yasuhiro Gifu University, Graduate School of Medicine, Department of Tumor Pathology, Research Associate, 大学院・医学研究科, 助手 (70313872)
HIROSE Yoshinobu Gifu University, School of Medicine, University Hospital, Associate Professor, 医学部付属病院, 助教授 (20293574)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥13,000,000 (Direct Cost: ¥13,000,000)
Fiscal Year 2004: ¥5,900,000 (Direct Cost: ¥5,900,000)
Fiscal Year 2003: ¥7,100,000 (Direct Cost: ¥7,100,000)
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| Keywords | Colon cancer / Apc gene / Min mouse / Premalignant lesion / p53 gene |
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| Research Abstract |
It is well known that Apc min mice develop intestinal tumors predominantly in the small intestine, but less number in the colon. In previous studies, we have identified the presence of a number of microadenomas in the colon of Apc min mice and showed that loss of heterozygosity of Apc is found in most of such microadenomas. These findings suggest that Apc LOH is responsible for microadenoma development, but is not sufficient for colon tumorigenesis. In order to identify alterations involved in promotion/progression stages of the carcinogenesis, we have performed mutational analysis and examined changes of protein expression in the colon tumors of Apc min mice. None of genetic alterations which are frequently found in human colon cancers, such as K-ras, p53 and B-raf gene mutations or microsatellite instability is not detectable at colon tumors in this model, suggesting that tumorigenesis process of this model is different from that of most human cancers. However, patterns of expression of many cancer-related proteins, such as PLK1, Aurora A, cyclin D1, Smad4, and MGMT which are identified by immunostainings are similar to those in human colon cancers, indicating the similarity of altered expressions between mice and humans. Further analyses are going on using genetically modified mouse models, combined with Apc min allele.
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Report
(3 results)
Research Products
(10 results)
