Journal Article

Acceleration of spontaneous biliary carcinogenesis in hamsters by bilioenterostomy

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

in Carcinogenesis

Volume 24, issue 1, pages 133-137
Published in print January 2003 | ISSN: 0143-3334
Published online January 2003 | e-ISSN: 1460-2180 | DOI:
Acceleration of spontaneous biliary carcinogenesis in hamsters by bilioenterostomy

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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.

Keywords: CD, choledochoduodenostomy; CJ, choledochojejunostomy; LI, labeling index; PCNA, proliferative cell nuclear antigen; SL, simple laparotomy; T-Bil, total bilirubin

Journal Article.  2911 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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