The involvement of mast cell in the progression of bladder cancer
| Project/Area Number |
15591672
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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 |
Urology
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| Research Institution | Teikyo University |
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Principal Investigator |
MUTO Satoru Teikyo University, School of Medicine, Department Urology, Associate Professor, 医学部, 講師 (30345194)
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| Co-Investigator(Kenkyū-buntansha) |
HORIE Shigeo Teikyo University, School of Medicine, Department Urology, Chairman & professor, 医学部, 教授 (40190243)
冨田 京一 東京大学, 医学部附属病院, 講師 (20272578)
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| Project Period (FY) |
2003 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2003: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | bladder cancer / inflammation / TNF / ras / 肥満細胞 / mast cell / Ras |
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| Research Abstract |
The rasH2 transgenic mice carry human c-Ha-ras proto-oncogene, and are highly susceptible to chemical carcinogenesis. Previous studies showed that the mutation of c-Ha-ras induced by DMBA in the tumors of rasH2 were detected only in transgenes. To examine if the difference of the codon of c-Ha-ras gene between human and mouse attributed to the tissue specific sensitivity to DMBA, we generated a line of transgenic mice, mras, carrying mouse c-Ha-ras genome with its own promoter. Western blot showed that the protein expression of H-RAS in the skin was increased in both rasH2 and mras compared with wild-type. Chemical skin carcinogenesis was induced by DMBA and TPA. In rasH2 mice, the latency of tumor formation was shorter than wild-type littermates. Both the number and the volume of skin tumors were increased in rasH2 than those of wild-type. However, in mras mice, enhancement of tumor formation was not observed as compared with wild-type. The mean number of tumors and the latency of tumor development was almost the same between mras and wild-type littermates. Mutational analysis showed only A to T transversion in human c-Ha-ras transgenes at the codon 61 but not in murine endogenous c-Ha-ras gene in the tumors of rasH2. While in the tumors of wild-type littermates and mras, A to T transversion in murine c-Ha-ras at the codon 61 were detected. These results indicate that the differences in the codon of c-Ha-ras gene between mice and human might attribute to the tissue specific sensitivity of DMBA.
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Report
(4 results)
Research Products
(7 results)
