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Title: Short communication: Promotion of cholangiocarcinogenesis in the hamster liver by bile duct ligation after dimethylnitrosamine initiation
Authors: Witaya Thamavit
Chawalit Pairojkul
Danai Tiwawech
Makoto Itoh
Tomoyuki Shirai
Nobuyuki Ito
Mahidol University
Khon Kaen University
National Cancer Institute Thailand
Nagoya City University
Keywords: Biochemistry, Genetics and Molecular Biology
Issue Date: 1-Nov-1993
Citation: Carcinogenesis. Vol.14, No.11 (1993), 2415-2417
Abstract: Administration of hepatocardnogenic nitrosamines before or after infection with the liver fluke, Opisthorchis viverrini (OV), results in marked development of cholangiocellular and hepatocellular precancerous and cancerous lesions in the hamster liver. The promoting effects of OV are believed to be exerted either mechanically, chemically or immuno-logically. To test the influence of possible mechanical effects, Syrian hamsters were initiated with a single i.p. injection of dimethylnitrosamine (DMN) 20 mg/kg and subjected 2 weeks later either to a sham operation or to complete ligation of the extrahepatic bile duct to the left lateral lobe. At the end of week 40, the animals receiving DMN-initiation and ligation had a 60.9% incidence of cholangiofibrosis, 21.7% of mucous cystadenomas and 39.1% of cholangiocarcinomas, whereas the group given DMN alone only developed cholangiofibrosis, limited to 5% of the animals. In the latter case neither cystadenomas nor cholangiocarcinomas were observed. The incidence of hepatocellular nodules did not differ between the two groups and no tumorous lesions developed in either the ligated or the untreated groups without DMN pretreatment. Complete ligation of the bile duct itself led to a series of events; obstruction of bile flow being followed by dilatation, cyst formation, and necrosis of the bile duct epithelium and surrounding affected areas leading to regenerative proliferation. The results are in line with the conclusion that parasite-associated proliferation in target cell populations is, at least in part, responsible for the influence of OV on liver tumor development. © 1993 Oxford University Press.
ISSN: 01433334
Appears in Collections:Scopus 1991-2000

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