In many tissues, carcinogenesis mimics embryonic development. This is true for 
the pancreas. The first alteration seen during pancreatic tumor induction in the 
hamster model is proliferation of poorly differentiated ductular (tubular) 
structures intermingled with endocrine cells, a pattern consistent with findings 
in the embryonic and fetal pancreas. However, unlike the fetal tissue, various 
cell types of intestinal epithelium appear in the advance stages of pancreatic 
carcinogenesis. Moreover, contrary to the situation in the fetal and adult 
hamster pancreas, the induced pancreatic lesion expresses antigens with human 
blood group type specificities, including A, B, H, Leb, Lex, and Ley, antigens 
that are expressed, however, by fetal and adult duodenal epithelium. Considering 
the origin of the pancreas from the duodenal mucosa, the overall findings 
indicate that during pancreatic carcinogenesis some genes, acquired from the 
progenitor (duodenal) cells, which are inactive in embryonic and normal 
pancreatic cells, are activated, possibly as a function of some oncogenes. 
Comparative studies in human tissue lead to the same conclusion.