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Inhibition by galanin of experimental carcinogenesis induced by azaserine in rat pancreas
Author(s) -
Iishi Hiroyasu,
Tatsuta Masaharu,
Baba Miyako,
Yano Hiroyuki,
Iseki Kazushige,
Uehara Hiroyuki,
Nakaizumi Akihiko
Publication year - 1998
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/(sici)1097-0215(19980130)75:3<396::aid-ijc12>3.0.co;2-7
Subject(s) - azaserine , galanin , pancreas , endocrinology , medicine , parenchyma , pancreatic cancer , somatostatin , carcinogenesis , biology , neuropeptide , pathology , cancer , biochemistry , receptor , amino acid , glutamine
The effects of galanin on pancreatic carcinogenesis induced by azaserine and on the norepinephrine concentration in the pancreas were investigated in male Wistar rats. Rats were given weekly injections of 10 mg/kg body weight of azaserine for 25 weeks and 8 μg/kg body weight of galanin in depot form every other day for 62 weeks. Azaserine‐induced pancreatic lesions were examined with hematoxylin and eosin and histochemical techniques. In week 62, quantitative histological examination showed that prolonged administration of galanin significantly reduced the number and size (as percent of parenchyma) of adenosine triphosphatase‐positive pancreatic lesions, which are correlated closely with the ultimate development of pancreatic cancer. The number of pancreatic adenocarcinomas in rats treated with galanin was significantly less than in controls. Galanin also significantly decreased the bromodeoxyuridine‐labeling index of azaserine‐induced pancreatic lesions and the norepinephrine concentration in the pancreas. Our findings indicate that galanin inhibits pancreatic carcinogenesis and that such inhibition may be related to the suppression of sympathetic nervous system activity and subsequently to the inhibition of cell proliferation in neoplastic lesions of the pancreas. Int. J. Cancer 75:396–399, 1998. © 1998 Wiley‐Liss, Inc.