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Effects of sandostatin and castration on pancreatic carcinogenesis in rats and hamsters
Author(s) -
Meuers M.,
Woutersen R. A.,
van GarderenHoetmer A.,
Barker G. H.,
de Jong F. H.,
Foekens J. A.,
Klijn J. G. M.
Publication year - 1992
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910500214
Subject(s) - azaserine , hamster , orchiectomy , pancreas , medicine , castration , endocrinology , somatostatin , carcinogen , gastrin , carcinogenesis , biology , hormone , cancer , biochemistry , amino acid , secretion , glutamine , genetics
The effects of treatment with the somatostatin analogue Sandostatin, separately and in combination with surgical castration, on the development of azaserine‐induced lesions in rat pancreas and N‐nitrosobis(2‐oxopropyl)amine (BOP)‐induced lesions in hamster pancreas were investigated. The animals were divided in 4 groups and treated as follows: (a) controls, injected s.c. with saline solution (0.9% NaCI); (b) orchiectomy directly after the last treatment with carcinogen; (c) Sandostatin (SMS 201–995) subcutaneously; (d) orchiectomy followed by treatment with Sandostatin. No significant suppressive effects on plasma EGF or IGF‐I concentrations were noted after Sandostatin treatment, but plasma gastrin levels decreased slightly in the rats, not in the hamsters. In rats, Sandostatin treatment enhanced rather than inhibited growth of acidophilic atypical acinar cell nodules. In hamster pancreas, by contrast, Sandostatin inhibited the development of putative pre‐neoplastic ductular lesions. There was no interaction between treatment with Sandostatin and surgical castration. It was concluded that Sandostatin, when administered prophylactically, has an inhibitory effect on the growth of putative pre‐neoplastic ductular, but not acinar, lesions.