Pancreatic carcinogenesis-enhancement by cholecystokinin in the hamster-nitrosamine model.
The role of the pancreaticotrophic hormone cholecystokinin (CCK) in modifying the pancreatic response to carcinogen has been examined in the hamster-nitrosamine pancreatic cancer model. Exogenous CCK, 30 IDU kg-1, stimulated a maximal pancreatic secretory response when given intravenously and caused hypertrophy and hyperplasia of the pancreas when given subcutaneously over a period of 6 weeks (pancreatic wet weight, mg per 100 g body weight, controls 295.6 +/- 61; CCK treated 466.4 +/- 77, P less than 0.001). When the same dose of CCK was given to animals receiving N-nitrosobis (2-oxopropyl)amine (BOP; 5 mg kg-1 weekly) there was a reduction in latency period and increase in induction rate of tumour development (CCK + BOP vs. BOP alone, 12 animals with tumours vs. 2 at 15 weeks; P less than 0.02). These effects are consistent with CCK acting as a co-carcinogen or promoter of pancreatic carcinogenesis in this model.
D000230:Adenocarcinoma / Q000139:chemically induced*; D000818:Animals; D002766:Cholecystokinin / Q000494:pharmacology / Q000633:toxicity*; D003043:Cocarcinogenesis; D006224:Cricetinae; D008297:Male; D008647:Mesocricetus; D009602:Nitrosamines / Q000633:toxicity*; D010179:Pancreas / Q000473:pathology; D010189:Pancreatic Juice / Q000378:metabolism; D010190:Pancreatic Neoplasms / Q000139:chemically induced*; D011230:Precancerous Conditions / Q000139:chemically induced / Q000473:pathology
D009602:Nitrosamines; C013622:nitrosobis(2-oxopropyl)amine; D002766:Cholecystokinin