Common variants in IL-1RN, IL-1β and TNF-α and the risk of ovarian cancer: a case control study

Autor: Amira Ben Ahmed, Sabrina Zidi, Ikram Sghaier, Ezzeddine Ghazouani, Amel Mezlini, Wassim Almawi, Besma Yacoubi Loueslati
Jazyk: angličtina
Rok vydání: 2017
Předmět:
Zdroj: Central European Journal of Immunology, Vol 42, Iss 2, Pp 150-155 (2017)
Druh dokumentu: article
ISSN: 1426-3912
1644-4124
DOI: 10.5114/ceji.2017.69356
Popis: Aim of the study: Several studies implicated altered inflammatory response in the susceptibility to ovarian cancer, and polymorphisms in inflammatory cytokines were shown to play an important role in the development of malignancies, including ovarian cancer (OC). Here we investigated the relationship between polymorphisms in IL-1 (-511C>T), IL-1RN VNTR, TNF- (-308G>A), and TNF RII (-322 VNTR) and OC risk in Tunisian women. Methods and results: Study subjects comprised 62 OC patients and 126 healthy women. Genotyping was done from genomic DNA obtained from blood simple by PCR. Positive association between IL-1RN (-VNTR) A1 allele (p = 0.0069; OR = 2.04; 95% CI:1.17-3.58) and OC risk, while negative association was seen with the A3 allele (P = 0.0034; OR = 0.09; 95% CI: 0.00-0.64), suggesting a protective role by the A3 allele. For IL-1 (-511C>T), homozygous C/C genotype was associated with significantly increased risk of OC (p = 0.0002; OR = 4.14; 95% CI: 1.77-9.76), while heterozygote C/T genotype was linked with reduced risk of OC (p = 0.0033; OR = 0.40; 95% CI: 0.20-0.78). Furthermore, TNF- -308A allele was significantly associated with heightened risk of OC (p = 0.016; OR = 1.70; 95% CI: 1.08-2.69), and homozygote G/G genotype was associated with decreased risk of OC (p = 0.0018; OR = 0.25; 95% CI: 0.09-0.66). In contrast, TNFRII (-322 VNTR) polymorphism was not associated with altered OC risk in the studied group. Conclusions: The significant association between IL-1RN VNTR, IL1- (-511), TNF- (-308) and OC susceptibility in Tunisian women confirms a role for altered inflammatory response in ovarian cancer pathogenesis.
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