From
Bench to Bedside:
Causation and Prevention
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The most consistently identified epidemiological risk factor for pancreatic cancer is cigarette smoking. A 2-10-fold risk of developing pancreatic cancer has been demonstrated for heavy smokers. In addition, there appears to be a potential relationship between the development of pancreatic cancer and environmental carcinogens, such as a high fat, low fier diet, industrial carcinogens, and radiation exposure. Most carcinogens need to be activated by drug-metabolizing enzymees into reactive molecules which can then exert their carcinogenic effect. Human pancreatic tissues have been shown to contain thse carcinogen-activating enzymes, such as nitrosamine compounds, which are present in both the human diet and cigarette smoke. These
compounds exert their carcinogenic effect by inducing damage
in DNA. We have demonstrated that damaged DNA can be detected
in human pancreatic cancers. This research is ongoing with
specific emphasis on developing a better understanding of
the relationship between cigarette smoking and the development
of pancreatic cancer at a molecular level. |
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Selected References: Wang M, Abbruzzese JL, Friess H, Hittelman WN, Evans DB, Abbruzzese MC, Chiao P,Donghi L. DNA adducts in human pancreatic tissues and their potential role in carcinogenesis. Cancer Res 1998;58:38-41. |