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Alteration of Pancreatic Endocrine Cell Patterns and Their Secretion during Pancreatic Carcinogenesis in the Hamster Model¹

The Eppley Institute for Research in Cancer and Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska [P. M. P.], and Veterans Administration Medical Center, University of Cincinatti, Cincinatti, Ohio [R. H. B.]

Proliferation of endocrine cells was found to occur during early, i.e., first 12 weeks, exocrine pancreatic carcinogenesis after 6 weekly treatments of Syrian hamsters with the pancreatic carcinogen N-nitrosobis(2-oxopropyl)amine (BOP). Cells containing insulin (Ins), glucagon (Glu), and somatostatin (Som) were noted in all stages of tumor development and were present in adenocarcinomas and in metastases to the liver. Some of the cancer cells were of amphicrine (hybrid) type, i.e., produced both mucin and endocrine substances. Measurement of these hormones revealed a significant decrease in plasma Ins during early stages of carcinogenesis with concomitant increase of Ins level in pancreatic juice at 12 weeks after 6 weekly BOP treatments. Plasma Glu and Som were not changed. The changes noted, particularly in relation to Ins, suggest that proliferation of endocrine cells in pancreatic carcinogenesis may be associated with alterations in hormone secretion.

¹ Supported by United States Public Health Service National Cancer Institute Grant CA38922, by Laboratory Core Grant CA36727, and by American Cancer Society Grant SIG-16.

² To whom requests for reprints should be addressed, at 42nd & Dewey Ave., Omaha, NE 68105.

Received 11/29/88. Revised 3/21/89. Revised 8/14/89. Accepted 8/18/89.