| Project/Area Number |
07670567
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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 |
Gastroenterology
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| Research Institution | UNIVERSITY of TOKYO |
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Principal Investigator |
KAWABE Takao University of Tokyo, Faculty of Medicine (Hospital) Associate, 医学部(病), 助手 (40195136)
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| Co-Investigator(Kenkyū-buntansha) |
KANAI Fmihiko University of Tokyo, Faculty of Medicine (Hospital), 医学部・附属病院, 医員
TADA Minoru University of Tokyo, Faculty of Medicine (Hospital), 医学部・附属病院, 医員
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1996: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1995: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | pancreas cancer / ras / point mutation / 遺伝子診断 / ras遺伝子 / 膵管過形成 / PCR |
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| Research Abstract |
A point mutation in the codon 12 of K-ras is detected in 70-80% of pancreas cancers. We previously showed this mutation in pancreatic juice in all the patients with pancreatic cancer using high sesitivite PCR.However, the mutations were also detected in pancreatic juice in 40% of the patients without cancer. We showed the mutation were derived from the hyperplasia of ductal epithelium. In pancratic cancer, the mutated codons were often GGT or TGT,whereas those in non-cancer patients were GGT or TGT.We were confirming this tendency in the further study using larger number of subjects. We also transfected mutated ras into the cells with wild-type ras, and investgated the growth, NDA synsesis, MAP-kinase activity and interaction with Raf 1-kinase in those cells. We continue to elicidate the relation of the mutation type to the cell phenotype, such as cancer, hyperplasia.
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