Interleukin-1 polymorphisms associated with increased risk of gastric cancer

Emad M. El-Omar (), Mary Carrington, Wong-Ho Chow, Kenneth E. L. McColl, Jay H. Bream, Howard A. Young, Jesus Herrera, Jolanta Lissowska, Chiu-Chin Yuan, Nathaniel Rothman, George Lanyon, Maureen Martin, Joseph F. Fraumeni and Charles S. Rabkin
Additional contact information
Emad M. El-Omar: National Cancer Institute
Mary Carrington: Intramural Research Support Program, Science Applications International Corporation Frederick, National Cancer Institute-Frederick Cancer Research and Development Centre
Wong-Ho Chow: National Cancer Institute
Kenneth E. L. McColl: Department of Medicine and Therapeutics Western Infirmary
Jay H. Bream: National Cancer Institute, Frederick Cancer Research and Development Centre
Howard A. Young: National Cancer Institute, Frederick Cancer Research and Development Centre
Jesus Herrera: Intramural Research Support Program, Science Applications International Corporation Frederick, National Cancer Institute-Frederick Cancer Research and Development Centre
Jolanta Lissowska: Cancer Centre and M. Sklodowska-Curie Institute of Oncology
Chiu-Chin Yuan: Intramural Research Support Program, Science Applications International Corporation Frederick, National Cancer Institute-Frederick Cancer Research and Development Centre
Nathaniel Rothman: National Cancer Institute
George Lanyon: Department of Medicine and Therapeutics Western Infirmary
Maureen Martin: Intramural Research Support Program, Science Applications International Corporation Frederick, National Cancer Institute-Frederick Cancer Research and Development Centre
Joseph F. Fraumeni: National Cancer Institute
Charles S. Rabkin: National Cancer Institute

Nature, 2000, vol. 404, issue 6776, 398-402

Abstract: Abstract Helicobacter pylori infection is associated with a variety of clinical outcomes including gastric cancer and duodenal ulcer disease1. The reasons for this variation are not clear, but the gastric physiological response is influenced by the severity and anatomical distribution of gastritis induced by H. pylori. Thus, individuals with gastritis predominantly localized to the antrum retain normal (or even high) acid secretion2, whereas individuals with extensive corpus gastritis develop hypochlorhydria and gastric atrophy3, which are presumptive precursors of gastric cancer4. Here we report that interleukin-1 gene cluster polymorphisms suspected of enhancing production of interleukin-1-beta are associated with an increased risk of both hypochlorhydria induced by H. pylori and gastric cancer. Two of these polymorphism are in near-complete linkage disequilibrium and one is a TATA-box polymorphism that markedly affects DNA–protein interactions in vitro. The association with disease may be explained by the biological properties of interleukin-1-beta, which is an important pro-inflammatory cytokine5 and a powerful inhibitor of gastric acid secretion6,7. Host genetic factors that affect interleukin-1-beta may determine why some individuals infected with H. pylori develop gastric cancer while others do not.

Date: 2000
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DOI: 10.1038/35006081

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