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Interleukin-6 and Interleukin-10 Gene Promoter Polymorphisms and Risk of Endemic Burkitt Lymphoma

机译:白细胞介素6和白细胞介素10基因启动子多态性与地方性伯基特淋巴瘤的风险

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摘要

Overexpression of interleukin-6 (IL-6) and IL-10 in endemic Burkitt lymphoma (eBL) may facilitate tumorigenesis by providing a permissive cytokine milieu. Promoter polymorphisms influence interindividual differences in cytokine production. We hypothesized that children genetically predisposed for elevated cytokine levels may be more susceptible to eBL. Using case-control samples from western Kenya consisting of 117 eBL cases and 88 ethnically matched healthy controls, we tested for the association between eBL risk and IL-10 (rs1800896, rs1800871, and rs1800872) and IL-6 (rs1800795) promoter single nucleotide polymorphisms (SNPs) as well as IL-10 promoter haplotypes. In addition, the association between these variants and Epstein Barr Virus (EBV) load was examined. Results showed that selected IL-10 and IL-6 promoter SNPs and IL-10 promoter haplotypes were not associated with risk eBL or EBV levels in EBV-seropositive children. Findings from this study reveal that common variants within the IL-10 and IL-6 promoters do not independently increase eBL risk in this vulnerable population.
机译:白细胞介素6(IL-6)和IL-10在地方性伯基特淋巴瘤(eBL)中的过表达可能通过提供允许的细胞因子环境来促进肿瘤发生。启动子多态性影响细胞因子产生的个体差异。我们假设遗传上倾向于细胞因子水平升高的儿童可能更易患eBL。使用来自肯尼亚西部的病例对照样本,其中包括117个eBL病例和88个种族匹配的健康对照,我们测试了eBL风险与IL-10(rs1800896,rs1800871和rs1800872)和IL-6(rs1800795)启动子单核苷酸之间的关联多态性(SNP)以及IL-10启动子单倍型。此外,检查了这些变体与爱泼斯坦巴尔病毒(EBV)负载之间的关联。结果显示,选择的IL-10和IL-6启动子SNP和IL-10启动子单倍型与EBV血清反应阳性儿童的风险eBL或EBV水平无关。这项研究的结果表明,IL-10和IL-6启动子内的常见变异不会独立增加该易感人群的eBL风险。

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