Histogenesis of experimental pancreatic carcinoma induced by DIPN in hamsters was studied morphologically and histologically. On the basis of carcinogenesis, two stages of changes in pancreatic tissue were seen: one being edematous which peaked at 8-10 weeks and the other being storomalfibrotic with acinous atrophy, resembling chronic pancreatitis. Hyperplastic changes (papillary hyperplasia and ductal proliferation) developed in the former stage, and atypical duct and adenomatous lesions (intraductal, tubular, papillary cystic and multilocular adenoma) were seen in the latter stage. In view of the histological resemblance of the stages, it was thought that hyperplastic changes develop into adenomatous lesions gradually. Pancreatic carcinomas, all of ductal origin, were seen at 16 weeks and after. Metastasis in regional lymph nodes and invasion of lymph and blood vessels were observed. According to the size of tumors and existence of infiltration, carcinomas were classified as infiltrated, minute and in situ carcinomas. Because of the similarity in the histological features, it was suggested that adenomas became infiltrated carcinomas, and intraductal adenomas or atypical ducts were the source of in situ carcinomas. However, minute carcinomas, in the absence of a precancerous lesion, were thought to be de novo in origin.