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Causation and Prevention

Smoking and Pancreatic Cancer

The most consistently identified epidemiological risk factor for pancreatic cancer is cigarette smoking. A 2- to 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 fiber diet, industrial carcinogens and radiation exposure. Most carcinogens need to be activated by drug-metabolizing enzymes into reactive molecules which can then exert their carcinogenic effect.

Human pancreatic tissues have been shown to contain these 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.                      

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.


© 2013 The University of Texas MD Anderson Cancer Center