title: Genetic variability in energy balance and pancreatic cancer risk in a population-based case-control study in Minnesota.
abstract: OBJECTIVE
  Accumulating evidence suggests that energy imbalance plays a role in pancreatic carcinogenesis. However, it remains unclear whether single-nucleotide polymorphisms (SNPs) in genes regulating energy homeostasis influence pancreatic cancer risk. We investigated this question in a case-control study conducted from 1994 to 1998.
  
  
  METHODS
  Patients (n = 173) were ascertained from hospitals in the Twin Cities and Mayo Clinic, Minnesota. Control subjects (n = 476) were identified from the general population and frequency matched to patients by age and sex. Seven SNPs were evaluated in relation to pancreatic cancer using unconditional logistic regression.
  
  
  RESULTS
  After adjustment for confounders, the leucine/proline or proline/proline genotype of the neuropeptide Y (NPY) gene rs16139 was associated with a lower risk than the leucine/leucine genotype (odds ratio, 0.40 [95% confidence interval, 0.15-0.91]). Conversely, an increased risk was observed for the glycine/arginine or arginine/arginine genotype of the adrenoceptor β2, surface (ADRB2) gene rs1042713 as compared with the glycine/glycine genotype (odds ratio, 1.52 [95% confidence interval, 1.01-2.31]).
  
  
  CONCLUSIONS
  This study first reveals that SNPs in genes modulating energy intake (NPY) and energy expenditure (ADRB2) altered pancreatic cancer risk. If confirmed by other studies, our findings may shed new light on the etiology and prevention of pancreatic cancer.
authors.affiliation: From the *Department of Epidemiology, Indiana University Richard M. Fairbanks School of Public Health at IUPUI; †Melvin Bren Simon Cancer Center, Indiana University, Indianapolis, IN; ‡Department of Biostatistics, Fay W. Boozman College of Public Health, University of Arkansas for Medical Sciences, Little Rock, AR; §Department of Molecular Biology, College of Life Sciences, Hebei United University, Tangshan, China; ∥Division of Epidemiology and Community Health, School of Public Health, and ¶Masonic Cancer Center, University of Minnesota, Minneapolis, MN.
authors.forename: Jianjun
authors.initials: J
authors.lastname: Zhang
authors.forename: Ishwori B
authors.initials: IB
authors.lastname: Dhakal
authors.forename: Xuemei
authors.initials: X
authors.lastname: Zhang
authors.forename: Anna E
authors.initials: AE
authors.lastname: Prizment
authors.forename: Kristin E
authors.initials: KE
authors.lastname: Anderson
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D004734:Energy Metabolism / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005838:Genotype; D054439:Ghrelin / Q000235:genetics; D006801:Humans; D007473:Ion Channels / Q000235:genetics; D020738:Leptin / Q000235:genetics; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D008910:Minnesota; D024101:Mitochondrial Proteins / Q000235:genetics; D009478:Neuropeptide Y / Q000235:genetics; D010190:Pancreatic Neoplasms / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide; D018343:Receptors, Adrenergic, beta-2 / Q000235:genetics; D022702:Receptors, Adrenergic, beta-3 / Q000235:genetics; D054411:Receptors, Leptin / Q000235:genetics; D012307:Risk Factors; D000071247:Uncoupling Protein 3
chemical_list: C553443:ADRB2 protein, human; C568534:ADRB3 protein, human; C515349:GHRL protein, human; D054439:Ghrelin; D007473:Ion Channels; D020738:Leptin; D024101:Mitochondrial Proteins; D009478:Neuropeptide Y; D018343:Receptors, Adrenergic, beta-2; D022702:Receptors, Adrenergic, beta-3; D054411:Receptors, Leptin; D000071247:Uncoupling Protein 3