Ahmed Amira Ben, Zidi Sabrina, Sghaier Ikram, Ghazouani Ezzeddine, Mezlini Amel, Almawi Wassim, Loueslati Besma Yacoubi
Department of Biology, Faculty of Sciences of Tunis, Laboratory of Mycology, Pathologies and Biomarkers: LR16ES05, El Manar University, Tunis, Tunisia.
Laboratory of Immunology, Military Hospital of Tunis, Tunis, Tunisia.
Cent Eur J Immunol. 2017;42(2):150-155. doi: 10.5114/ceji.2017.69356. Epub 2017 Aug 8.
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.
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.
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.
多项研究表明炎症反应改变与卵巢癌易感性有关，炎症细胞因子的多态性在包括卵巢癌（OC）在内的恶性肿瘤发生发展中起重要作用。在此，我们研究了白细胞介素-1（-511C>T）、白细胞介素-1受体拮抗剂可变数目串联重复序列（IL-1RN VNTR）、肿瘤坏死因子-α（-308G>A）和肿瘤坏死因子受体II（-322 VNTR）的多态性与突尼斯女性卵巢癌风险之间的关系。
研究对象包括62例卵巢癌患者和126例健康女性。通过聚合酶链反应（PCR）从血液样本中提取的基因组DNA进行基因分型。白细胞介素-1受体拮抗剂（-VNTR）A1等位基因与卵巢癌风险呈正相关（p = 0.0069；比值比[OR]=2.04；95%置信区间[CI]：1.17 - 3.58），而A3等位基因与卵巢癌风险呈负相关（P = 0.0034；OR = 0.09；95% CI：0.00 - 0.64），提示A3等位基因具有保护作用。对于白细胞介素-1（-511C>T），纯合子C/C基因型与卵巢癌风险显著增加相关（p = 0.0002；OR = 4.14；95% CI：1.77 - 9.76），而异合子C/T基因型与卵巢癌风险降低相关（p = 0.0033；OR = 0.40；95% CI：0.20 - 0.78）。此外，肿瘤坏死因子-α -308A等位基因与卵巢癌风险显著升高相关（p = 0.016；OR = 1.70；95% CI：1.08 - 2.69），纯合子G/G基因型与卵巢癌风险降低相关（p = 0.0018；OR = 0.25；95% CI：0.09 - 0.66）。相比之下，肿瘤坏死因子受体II（-322 VNTR）多态性与研究组卵巢癌风险改变无关。
突尼斯女性中白细胞介素-1受体拮抗剂可变数目串联重复序列、白细胞介素-1（-511）、肿瘤坏死因子-α（-308）与卵巢癌易感性之间的显著关联证实了炎症反应改变在卵巢癌发病机制中的作用。
