Abstract
This chapter describes animal carcinogens and the two predominant experimental animal models of pancreatic cancer, including recently observed oncogenetic alterations. It summarizes the body of evidence obtained in human carcinogenesis, that is, findings from molecular biology and observational epidemiology. The chapter compares animal and human data for oncogenetic events, several lifestyle factors, and diabetes. One of the main characteristics of tumor growth is increased cell proliferation. Cell proliferation correlates positively with the development of pre-neoplastic pancreatic lesions in both rats and hamsters. Cell proliferation in putative preneoplastic lesions in rat pancreas can be modulated by dietary raw soya flour and dietary fish oil. Raw soybean flour and trypsin inhibitors have been implicated as nongenotoxic pancreatic carcinogens. The majority of epidemiological investigations in different populations using different designs have implicated smoking in the etiology of cancer of the pancreas. In 1986, the evidence of an association between the drinking of alcohol and the development of cancer of pancreas was judged insufficient.
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