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© 1983 Oxford University Press

research-article

Modification of pancreatic carcinogenesis in the hamster model. 5. Effect of partial pancreatico-colostomy

Parviz M. Pour, Katla Donnelly and Katherine Stepan

Eppley Institute for Research in Cancer, Department of Pathology and Laboratory Medicine and Department of Microbiology, University of Nebraska Medical Center Omaha, NE 68105, USA

Studies were conducted to evaluate the possibility of a bile reflux mechanism in the etiology of induced pancreatic cancer. N-Nitrosobis(2-oxopropyl)amine (BOP) was administered to Syrian hamsters after partial pancreatico-colostomy. Either the gastric or the splenic lobe of the pancreas was anastomosed to the transverse colon in groups 1 and 2, respectively. Group 3 were sham-operated controls and group 4 were controls without surgery. Shortly after surgery all 4 groups received a single subcutaneous BOP injection (20 mg/kg body weight) and survivors were sacrificed 46 weeks after BOP treatment. BOP-induced pancreatic tumor patterns were not altered by pancreatico-colostomy when compared with those in sham-operated controls. In all BOP treated hamsters the number and distribution of benign and malignant lesions were similar in each individual pancreatic segment, including the anastomosed lobe (A-lobe); some hamsters developed tumors only in the A-lobe. As in other pancreatic regions, the initial hyperplasia in the A-lobe primarily affected peri- and intra-insular ductules and less frequently involved the ducts. These findings support the theory that the carcinogen is bloodborne and indicate that BOP responsive pancreatic cells are distributed on a volume basis in distinct proportions within the pancreatic segments. As in previous experiments a higher incidence of pancreatic neoplasms was found in BOP-treated controls (those not operated upon) than in partially pancreatico-colostomized hamsters, including those with sham operations. Hyperplastic and dyplastic development of colonic mucosa around the anastomosis could be related to a local effect of carcinogen or of its metabolites, which are known to be excreted via pancreatic secretions.


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