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Interleukin-1 polymorphisms associated with increased risk of gastric cancer

Author

Listed:
  • Emad M. El-Omar

    (National Cancer Institute
    Department of Medicine and Therapeutics Aberdeen University)

  • 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)

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.

Suggested Citation

  • 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 & Maur, 2000. "Interleukin-1 polymorphisms associated with increased risk of gastric cancer," Nature, Nature, vol. 404(6776), pages 398-402, March.
    • Handle: RePEc:nat:nature:v:404:y:2000:i:6776:d:10.1038_35006081
    DOI: 10.1038/35006081
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    Cited by:

    1. Hong-Bae Kim & Jae-Yong Shim & Byoungjin Park & Yong-Jae Lee, 2018. "Long-Term Exposure to Air Pollutants and Cancer Mortality: A Meta-Analysis of Cohort Studies," IJERPH, MDPI, vol. 15(11), pages 1-15, November.
    2. Ji Yeong Yang & Pumsoo Kim & Seok-Hoo Jeong & Seong Woong Lee & Yu Sik Myung & Myong Ki Baeg & Jong-Bae Kim, 2020. "The Effects of Sulglycotide on the Adhesion and the Inflammation of Helicobacter Pylori," IJERPH, MDPI, vol. 17(8), pages 1-9, April.

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