Weekly s.c. injections of equitoxic doses of 2-hydroxy-propyl-n-propylnitrosamine, 2-oxopropyl-n-propylnitrosamine, and methyl-n-propylnitrosamine, assumed metabolites of di-n-propylnitrosamine by beta oxidation, induced low incidences of pancreatic duct adenomas in Syrian golden hamsters. Di-n-propylnitrosamine did not. Application of 2,2'-dihydroxydi-n-propylnitrosamine, another postulated intermediate of di-n-propylnitrosamine, led to development of various types of pancreatic duct adenomas and ductal carcinomas in high percentages of hamsters. In addition, a few acinar-cell carcinomas were found. The morphology of these neoplasms, their latencies, and their distribution in the different segments of the pancreas are described.

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