Carcinogenesis, Vol 18, 315-320, Copyright © 1997 by Oxford University Press
M Chu, JF Rehfeld and K Borch
In order to examine the effect of cholecystokinin on spontaneous and
induced pancreatic carcinogenesis in the hamster, two sets of experiments
were carried out, one involving long-term hypercholecystokininemia and one
involving cancer induction during hypercholecystokininemia. The effect of
hypercholecystokininemia, induced by pancreaticobiliary diversion (PBD),
was studied for 8 months. Neither PBD animals nor sham-operated controls
developed premalignant or malignant pancreatic lesions. However, in the PBD
group the mean pancreatic weight, total protein content and DNA content
were increased by 30, 29 and 27% respectively. No such increases were found
in PBD animals receiving a cholecystokinin-A receptor antagonist during the
last 24 days of the experiment. In the cancer induction study, the effect
of PBD on N-nitrosobis(2-oxopropyl)amine-induced pancreatic carcinogenesis
was studied for 3 months. Putative premalignant pancreatic lesions were
diagnosed in all PBD hamsters and in four of 15 sham-operated controls.
Pancreatic ductular carcinoma in situ was only found in PBD animals. The
[3H]thymidine labeling index of the pancreatic lesions was significantly
higher in the PBD group than in the controls. No such increase was observed
in PBD animals receiving a cholecystokinin-A receptor antagonist during the
last 5 days of the experiment. It is concluded that chronic endogenous
hypercholecystokininemia promotes early phase pancreatic carcinogenesis,
but does not per se cause development of premalignant or malignant
pancreatic lesions in the hamster.
ARTICLES
Chronic endogenous hypercholecystokininemia promotes pancreatic carcinogenesis in the hamster
Department of Surgery, University Hospital of Linkoping, Sweden.
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