Inhibitory effect of streptozotocin on tumor development in transgenic mice bearing an elastase I-SV40 T-antigen fusion gene.
Transgenic mice, bearing a fusion gene of rat elastase I promoter and SV40 T-antigen, developed acinar cell tumors of the pancreas, as predicted by the model. In addition, they developed insulinomas and somatostatin (delta)-cell hyperplasia of the pancreatic islets. The insulinomas and the delta-cell hyperplasia appeared to be functional, as evidenced by changes in plasma glucose, insulin, and somatostatin. Streptozotocin, which has been shown to inhibit pancreatic carcinogenesis in the hamster model, significantly reduced the numbers of insulinomas and delta-cell hyperplasias. Streptozotocin did not cause a statistically significant reduction in exocrine tumors.
Department of Pathology, Dartmouth Medical School, Hanover, New Hampshire 03756.
R H
RH
Bell
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T
Brinck-Johnsen
D S
DS
Longnecker
D000818:Animals; D000952:Antigens, Polyomavirus Transforming / Q000235:genetics*; D001786:Blood Glucose / Q000032:analysis; D002471:Cell Transformation, Neoplastic / Q000187:drug effects* / Q000235:genetics; D003001:Cloning, Molecular; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000150:complications; D005260:Female; D006965:Hyperplasia / Q000453:epidemiology / Q000209:etiology / Q000473:pathology; D007328:Insulin / Q000097:blood; D007340:Insulinoma / Q000453:epidemiology / Q000209:etiology / Q000473:pathology; D008297:Male; D051379:Mice; D008822:Mice, Transgenic / Q000235:genetics*; D010196:Pancreatic Elastase / Q000235:genetics*; D010190:Pancreatic Neoplasms / Q000453:epidemiology / Q000209:etiology / Q000473:pathology; D012307:Risk Factors; D013004:Somatostatin / Q000097:blood; D013311:Streptozocin / Q000494:pharmacology*
D000952:Antigens, Polyomavirus Transforming; D001786:Blood Glucose; D007328:Insulin; D013004:Somatostatin; D013311:Streptozocin; D010196:Pancreatic Elastase