| Project/Area Number |
06671220
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
General surgery
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| Research Institution | KYOTO PREFECTURAL UNIVERSTIY OF MEDICINE |
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Principal Investigator |
TOKIWA Kazuaki KYOTO PREFECTURAL UNIVERSITY OF MEDICINE,ASSISTANT PROFESSOR, 医学部, 助手 (30163968)
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| Co-Investigator(Kenkyū-buntansha) |
OGITA Shuhei KYOTO PREFECTURAL UNIVERSTIY OF MEDICINE,ASSCIATE PROFESSOR, 医学部, 講師 (20128698)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1994: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | ANOMALOUS ARRANGEMENT OF THE PANCREATICOBILIARY DUCT / CARCINOGENESIS / BILE ACIDS / PANCREATIC ENZYME |
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| Research Abstract |
Anomalous arrangement of the pancreaticobiliary duct (AAPBD) is frequently associated with biliary tract malignancies. The aim of this study was to determine the promoting factors in the pathogenesis of biliary tract carcinoma.
In the study of bile obtained from AAPBD patients, the mean of bile acid concetration was significantly lower than of control patiets. Non conjugated bile acids and secondary bile acids were found in these bile from AAPBD patients, while bile acids were not found in bile from control patients. These results suggest that non conjugated and secondary bile acids play a part in tumor promotion of bile duct carcinogenesis in patients with AAPBD.
Then we investigated the effects on cellular functions of bile acid and trypsin using a chick embryo fibroblast culture system. Bile acid was found to increase PGE_2 synthesis which has been shown to be increased in premalignant lesions, but to suppress the incorporation of [^3H] TdR into DNA.On the other hand, trypsin increased the incorporation of [^3H] TdR into DNA,but did not increase PGE_2 synthesis. These results suggest that both the bile acid and trypsin present in the bile juice in AAPBD act to stimulate cell proliferation, but that their mechanisms of action on cell growth differ.
In conclusion, the combination of effects of different types of tumor promoters in the stagnant bile juice in AAPBD may account for the high incidence of carcinogenesis. Further study of various components of stagnant bile juice other than bile acids and trypsin should also be carried out.
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