Cell differentiation during pancreatic carcinogenesis.

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.