Pancreatic cancer is the fifth most common cause of death due to
cancer. Except for an association with cigarette smoking, its etiology is poorly understood. Because of the dearth of epidemiological clues as to causation, studies with experimental animal models assume greater importance. Rodent models of
pancreatic cancer indicate that while
dietary fat per se does not cause
pancreatic cancer, it does enhance or promote
tumor development. Subsequent to treatment with a pancreatic
carcinogen, high intakes of dietary
unsaturated fats of the n-6 series, but not saturated
fats, enhance or promote
tumor development. A requisite level of
linoleic acid is needed for this promotion.
Fats of the n-3 series (e.g., certain
fish oils) are inhibitory to
tumor growth. Promotion by
dietary fats appears only partly related to the high caloric content of fat. Mechanistically, certain dietary
unsaturated fats appear to selectively enhance the growth rate of
carcinogen-induced, pre-cancerous lesions. Irrespective of precise understanding of mechanisms of promotion, it appears possible to intervene in the process of
cancer development and reduce the burden of
cancer. Experimentally, this may be accomplished by decreasing total fat intake, decreasing caloric intake, increasing exercise or increasing the intake of
n-3 fatty acids.