| Project/Area Number |
09671242
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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 |
General surgery
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| Research Institution | KYOTO PREFECTURAL UNIVERSITY OF MEDICINE |
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Principal Investigator |
TOKIWA Kazuaki KYOTO PREFECTURAL UNIVERSITY OF MEDICINE,ASSISTANT PROFESSOR, 医学部, 助教授 (30163968)
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| Co-Investigator(Kenkyū-buntansha) |
OGITA Shuhei KYOTO PREFECTURAL UNIVERSITY OF MEDICINE,ASSOCIATE PROFESSOR, 医学部, 講師 (20128698)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1998: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1997: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | ANOMALOUS ARRANGEMENT OF THE PANCREATICOBILIARY DUCT / CARCINOGENESIS / BILE ACIDS / PANCREATIC ENZYME / MOLECULAR BIOLOGY / 膵酸素 |
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| Research Abstract |
Anomalous arrangement of the pancreaticobiliary duct (AAPBD) is an anatomical maljunction of the bile duct and the pancreatic duct that is frequently associated with biliary tract malignancies. The purpose of this study was to clarify the mechanism of carcinogenesis in patients with AAPBD with special reference to molecular biology.
We histologically examined gallbladder specimens obtained from pediatric patients with AAPBD, and showed that mucosal hyperplasia was frequently observed in the gallbladder in children with AAPBD but not in children without this anomaly. Moreover, the incidence of epithelial hyperplasia was significantly increased in the gallbladder of children in whom the pancreatic duct joined the common bile duct (P-C type) compared with that of children in whom the common bile duct joined the pancreatic duct (C-P type). In addition, cell kinetic studies have demonstrated increased cellular proliferative activity of the gallbladder in children with AAPBD.The activity of cell proliferation was significantly elevated in children with the P-C type of AAPBD compared with that in children with the C-P type of anomaly. p53 gene overexpression was not noted in the gallbladder of children with AAPBD.Then we investigated the effects on biliary carcinogenesis of bile acid and trypsin using gallbladder carcinoma inducad by 3-methvlcholanthrene in hamsters. Bile acid and trypsin were found to increase the incidence of gallbladder carcinoma in hamsters. p53 gene overexpression was demonstrated in cancerous areas in about 40 % of animal gallbladder carcinoma.
These results suggest that the combination effects of bile acid and pancreatic enzymes in the stagnant bile activate cellular function of the gallbladder mucosa in patients with AAPBD.However, further studies are needed to determine genetic alterations involved in gallbladder carcinogenesiS in patients with AAPBD.
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