Abstract
Abstract A95 Pancreatic cancer is one of the leading causes of cancer death in developed countries. Although the etiology of pancreatic cancer remains elusive, based on epidemiologic studies, obesity and type-2 diabetes appear to increase risk of this fatal disease. Therefore, it is possible that polymorphisms in genes involved in energy metabolism modulate pancreatic cancer risk. We investigated this hypothesis using a case-control study conducted during 1994-1998 in Minnesota. Cases (n=189), aged 20 years or older, were ascertained from all hospitals in the metropolitan area of the Twin Cities and the Mayo Clinic; from the later, only cases residing in the Upper Midwest of the US were recruited. Controls (n=486) were randomly selected from the general population and frequency matched to cases by age (within 5 years) and sex. Polymorphisms in four genes were genotyped: leptin (LEP, -2548G>A, rs7799039), leptin receptor (LEPR, Gln223Arg, rs1137101), and neuropeptide Y (NPY, Leu7Pro, rs16139) (regulating energy intake), and β2-adrenoceptor (ADRB2, Gly16Arg, rs1042713) (regulating energy expenditure). Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated using unconditional logistic regression. After adjustment for age, sex, race, education, cigarette smoking, and alcohol use, a statistically significantly reduced risk of pancreatic cancer was observed in subjects who were heterozygous or homozygous for the NPY7Pro allele as compared with those who were homozygous for the NPY7Leu allele) [OR (95%CI): 0.39 (0.15-0.89)]. The variant allele (16Arg) of ADRB2 was associated with a borderline significantly increased risk [OR (95%CI): 1.47 (0.99-2.21)]. No appreciable effects were detected for the LEP and LEPR sequence variants examined. The genetic associations described above were not markedly modified by physical activity or dietary intake of energy, fat, or fiber. This study offers novel data suggesting that genetic variability in the regulation of energy intake and expenditure influences pancreatic cancer risk. Citation Information: Cancer Prev Res 2008;1(7 Suppl):A95.
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