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J Natl Cancer Inst. 1983 Sep;71(3):607-13.

Modification of pancreatic carcinogenesis in the hamster model. IX. Effect of pancreatitis.


The effect of acute and recurrent pancreatitis was investigated in pancreatic cancer induction by N-nitrosobis(2-oxopropyl)amine (BOP) in Syrian golden hamsters. For the correlation of the cellular alteration with carcinogenesis, BOP (20 mg/kg body wt) was injected once sc into hamsters at day 3 (group 2), week 1 (group 3), and week 8 (group 4), corresponding to cellular degeneration, regeneration, and healing, respectively. Additional groups received BOP 30 minutes before common duct ligation for 48 hours (group 1) or before repeated induction of pancreatitis at 4 weekly intervals for 4 weeks (group 5). Group 6 was a pancreatitis control. Two groups of hamsters received BOP only, at the age of 8 weeks (group 7, which served as a BOP control for groups 1-3 and 5) or at the age of 16 weeks (group 8, the control for group 4). Hamsters were killed 46 weeks after BOP injection (with the exception of group 1 animals, which were killed 52 wk after BOP) to guarantee the same postcarcinogen exposure time in each group. The results showed that BOP, when given during cellular degeneration (group 2) and healing (group 4), induced significantly fewer carcinomas than in the control groups, whereas the tumor pattern was not affected when BOP was given before pancreatitis induction (group 1) or at the time of cellular regeneration (group 3). Recurrent pancreatitis (group 5), however, resulted in carcinomas significantly larger in number and size than those in control group 8. A significantly higher incidence of carcinomas occurred in group 8 controls (treated with BOP at the age of 16 wk) compared to the incidence in group 7 controls (treated with BOP at the age of 8 wk).

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