An Overview of Genetic Polymorphisms and Pancreatic Cancer Risk in Molecular Epidemiologic Studies

  • Lin Yingsong
    Department of Public Health, Aichi Medical University School of Medicine
  • Yagyu Kiyoko
    Department of Public Health, Aichi Medical University School of Medicine
  • Egawa Naoto
    Department of Internal Medicine, Tokyo Metropolitan Komagome Hospital
  • Ueno Makoto
    Hepatobiliary and Pancreatic Medical Oncology Division, Kanagawa Cancer Center Hospital
  • Mori Mitsuru
    Department of Public Health, Sapporo Medical University School of Medicine
  • Nakao Haruhisa
    Division of Gastroenterology, Department of Internal Medicine, Aichi Medical University School of Medicine
  • Ishii Hiroshi
    Hepatobiliary and Pancreatic Section, Gastroenterological Division, Cancer Institute Hospital
  • Nakamura Kozue
    Department of Epidemiology and Preventive Medicine, Gifu University Graduate School of Medicine
  • Wakai Kenji
    Department of Preventive Medicine, Nagoya University Graduate School of Medicine
  • Hosono Satoyo
    Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute
  • Tamakoshi Akiko
    Department of Public Health, Aichi Medical University School of Medicine
  • Kikuchi Shogo
    Department of Public Health, Aichi Medical University School of Medicine

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Background: Although pancreatic cancer has been extensively studied, few risk factors have been identified, and no validated biomarkers or screening tools exist for early detection in asymptomatic individuals. We present a broad overview of molecular epidemiologic studies that have addressed the relationship between pancreatic cancer risk and genetic polymorphisms in several candidate genes and suggest avenues for future research.<BR>Methods: A comprehensive literature search was performed using the PubMed database.<BR>Results: Overall, individual polymorphisms did not seem to confer great susceptibility to pancreatic cancer; however, interactions of polymorphisms in carcinogen-metabolizing genes, DNA repair genes, and folate-metabolizing genes with smoking, diet, and obesity were shown in some studies. The major problem with these studies is that, due to small sample sizes, they lack sufficient statistical power to explore gene–gene or gene–environment interactions. Another important challenge is that the measurement of environmental influence needs to be improved to better define gene–environment interaction. It is noteworthy that 2 recent genome-wide association studies of pancreatic cancer have reported that variants in ABO blood type and in 3 other chromosomal regions are associated with risk for this cancer, thus providing new insight into pancreatic cancer etiology.<BR>Conclusions: As is the case in other complex diseases, common, low-risk variants in different genes may act collectively to confer susceptibility to pancreatic cancer in individuals with repeated environmental exposures, such as smoking and red meat intake. Clarification of gene–gene and gene–environmental interaction is therefore indispensable for future studies. To address these issues, a rigorously designed molecular epidemiologic study with a large sample is desirable.

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