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Carcinogenesis, Vol. 24, No. 1, 133-137, January 2003
© 2003 Oxford University Press

CARCINOGENESIS

Acceleration of spontaneous biliary carcinogenesis in hamsters by bilioenterostomy

Tomoo Kitajima1, Yoshitsugu Tajima, Sumihiro Matsuzaki, Tamotsu Kuroki, Kenzou Fukuda and Takashi Kanematsu

Department of Surgery II, Nagasaki University School of Medicine, Nagasaki, Japan and Goto Central Hospital, 205 Yoshikugi, Fukue 853-0031, Japan

Biliary carcinomas can occur as a delayed complication of bilioenterostomy. The aim of this study was to determine whether bilioenterostomy influences biliary carcinogenesis in hamsters. Syrian hamsters were subjected to three different surgical procedures: simple laparotomy (SL), choledochoduodenostomy (CD) and choledochojejunostomy (CJ). They were given no carcinogens, and five to six hamsters from each group were killed every 20 weeks up to 120 weeks after surgery. Thirty-seven, 32 and 38 hamsters were sampled from the SL, CD and CJ groups, respectively. Cholangiocarcinomas developed in 5.4, 15.6 and 23.7% of hamsters in the SL, CD and CJ groups, respectively. The incidence of biliary carcinoma was significantly higher in the bilioenterostomy groups, especially CJ (P < 0.05), than in SL. The tumor latency period after surgery was 20–40 weeks shorter in the bilioenterostomy groups than in SL. Persistent cholangitis and bile stasis were frequent in the bilioenterostomy groups, and a significant correlation between cholangitis and biliary carcinogenesis was noted in the CD group. The proliferative cell nuclear antigen (PCNA) labeling index was higher in the biliary epithelium of the bilioenterostomy groups. In conclusion, persistent cholangitis after bilioenterostomy accelerates biliary carcinogenesis through activation of biliary epithelial cell kinetics.


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