Genetic polymorphism of interleukin-17A and -17F genes in gastric carcinogenesis
Interleukin-17A (IL-17A) and IL-17F play a role in tissue inflammation by inducing release of proinflammatory and neutrophil-mobilizing cytokines. We investigated the associations between gastric cancer and polymorphisms of IL-17A (rs2275913, G-197A) and -17F (rs763780, 7488 T/C) genes. The study wa...
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Published in | Human immunology Vol. 70; no. 7; pp. 547 - 551 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.07.2009
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Subjects | |
Online Access | Get full text |
ISSN | 0198-8859 1879-1166 1879-1166 |
DOI | 10.1016/j.humimm.2009.04.030 |
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Summary: | Interleukin-17A (IL-17A) and IL-17F play a role in tissue inflammation by inducing release of proinflammatory and neutrophil-mobilizing cytokines. We investigated the associations between gastric cancer and polymorphisms of
IL-17A (rs2275913, G-197A) and
-17F (rs763780, 7488 T/C) genes. The study was performed in 811 subjects (524 without gastric cancer and 287 with gastric cancer). We used the multiplex PCR-SSCP method to detect gene polymorphisms. Overall, the number of
IL-17A/−197A allele was significantly correlated to the development of gastric cancer (OR, 1.42; 95% CI, 1.09–1.85;
p = 0.010). The frequency of
IL-17A/−197 A/A homozygote was also significantly higher in gastric cancer group than in non-cancer group (OR, 3.02; 95% CI, 1.86–4.91;
p < 0.0001). The IL-17A/G-197A polymorphism was more closely correlated to intestinal-type cancer than diffuse-type cancer. In addition,
IL-17A/−197A allele carriers had an increased risk of the development of gastric mucosal atrophy (OR, 1.68; 95% CI, 1.06–2.65;
p = 0.026), and a positive relationship between the inflammation score and the number of −197A allele was observed (
p = 0.022). We concluded that G-197A polymorphism of
IL-17A gene was significantly associated with the development of gastric cancer, especially intestinal-type cancer. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0198-8859 1879-1166 1879-1166 |
DOI: | 10.1016/j.humimm.2009.04.030 |