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Int J Mol Epidemiol Genet 2011;2(3):236-244

Original Article
Sequence variants in antioxidant defense and DNA repair genes, dietary
antioxidants, and pancreatic cancer risk

Jianjun Zhang, Xuemei Zhang, Ishwori B. Dhakal, Myron D. Gross, Fred F. Kadlubar, Kristin E. Anderson

Division of Epidemiology, Department of Public Health, Indiana University School of Medicine, Indianapolis, IN, USA: Division of
Medical Genetics, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR, USA; Division of
Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN, USA; Department of
Laboratory Medicine and Pathology, School of Medicine, University of Minnesota, Minneapolis, MN, USA>

Received May 4, 2011; accepted May 25, 2011; Epub June 5, 2011; published August 30, 2011

Abstract: To investigate whether polymorphisms in genes related to oxidative stress act alone or in combination with
antioxidants to modulate pancreatic cancer risk.  Cases (n=189), ages ≥ 20 years, were ascertained in 1994-1998 from all
hospitals in the Twin Cities and the Mayo Clinic. Controls (n=486) were randomly selected from the general population and
frequency matched to cases by age and sex.  After adjustment for confounders, individuals who were homozygous or
heterozygous for the variant allele of SOD2 polymorphism (Ala16Val, rs4880) experienced a 43% lower risk than those who
were homozygous for the wild-type allele [OR (95% CI): 0.57 (0.37, 0.89)]. Conversely, an increased risk was observed for the
variant allele of hOGG1 polymorphism (Ser326Cys, rs1052133) compared with the wild-type allele [OR (95% CI) for Ser/Cys or
Cys/Cys vs. Ser/Ser: 1.57 (1.04, 2.39)]. The protective effect of the variant allele of SOD2 was more pronounced among subjects
with a low dietary intake (<median) of lutein/zeaxanthin, lycopene, α-carotene, and α-tocopherol [OR (95% CI): 0.46 (0.27, 0.81),
0.42 (0.23, 0.75), 0.47 (0.26, 0.85), and 0.48 (0.27, 0.87), respectively].  Individual variations in the capacity to defend against
oxidative stress and to repair oxidative DNA damage influence pancreatic cancer risk, and some of these genetic effects are
modified by dietary antioxidants.(IJMEG1105001).

Key words: Antioxidants, DNA repair, oxidative stress, pancreatic cancer, polymorphisms

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Address all correspondence to:
Jianjun Zhang, MD, PhD
Division of Epidemiology
Department of Public Health
Indiana University School of Medicine
714 N Senate Avenue, Suite EF209
Indianapolis, IN 46202
Phone: (317) 274-4287
Fax: (317) 274-3443
Email: jz21@iupui.edu