O. Ishikawa et al., THE ROLE OF PANCREATIC-ISLETS IN EXPERIMENTAL PANCREATIC CARCINOGENICITY, The American journal of pathology, 147(5), 1995, pp. 1456-1464
Our previous studies have suggested that the presence of intact islets
is essential for the induction of pancreatic exocrine tumors in the S
yrian hamster model. To validate this, we investigated the effect of t
he carcinogen, N-nitrosobis(2-oxo-propyl)amine (BOP) in hamsters, in w
hich homologous isolated intact islets were transplanted into the subm
andibular gland (SMG). Freshly isolate pure islets for hamster donors
were transplanted into the left SMG of 20 female host hamster. Ten of
these hamsters (group 1) received BOP (40 mg/kg) weekly for 3 weeks. A
nother 10 hamsters (group 2) were kept untreated. In groups 3 and 4 (1
0 hamsters each) the salt solution or isolated pancreatic ductal cells
, respectively, was injected into the gland. In other groups (10 hamst
ers each) islets were transplanted into the peri-SMG connective tissue
(group 5) or into the renal subcapsular space (group 6). Hamsters of
groups 3 to 6 were treated with BOP as in group 1 (40 mg/kg, weekly fo
r 3 weeks) as were group 7 hamsters, which served as BOP-treated contr
ols. All BOP-treated hamsters developed pancreatic lesions. Similar hy
perplastic and atypical ductal/ductular proliferation and in situ carc
inoma were found in the SMG of many group 1 hamsters. No such lesions
were found in the SMG, peri-SMG, or renal subcapsular space of the oth
er groups. Islets appear to be involved in carcinogenicity of BOP. The
mechanism is obscure.