No Association between Circulating Levels and Genetic Variants of IL-6 and TNF-α and Colon Adenoma.

No Association between Circulating Levels and Genetic Variants of IL-6 and TNF-α and Colon Adenoma.
复制标题

DOI:
10.4021/gr529w
复制
发表时间:
2013-04
影响因子:
1.5
通讯作者:
Li L
Li L
中科院分区:
其他
文献类型:
--
作者:
Vaughn CB;Ochs-Balcom HM;Nie J;Chen Z;Thompson CL;Tracy R;Li L

文献摘要

相似文献

白细胞介素6(IL-6)和肿瘤坏死因子α(TNF-α)是两种重要的炎性细胞因子,在流行病学研究中与结肠肿瘤的风险存在不一致的相关性。然而,迄今为止的研究尚未充分评估这些细胞因子的生物标志物和遗传变异与结直肠腺瘤(结直肠癌的前体病变)之间的关联是否存在种族特异性差异。我们试图确定IL-6和TNF-α的循环水平或IL-6和TNF-α的遗传多态性是否与结肠腺瘤相关,如果是,这种相关性是否因种族而异。我们在一项基于结肠镜检查的病例对照研究中分析了循环水平和IL-6和TNF-α的单核苷酸多态性(SNP)与结肠腺瘤风险的关系,该研究包括401例新发腺瘤病例和1,050例对照。我们使用多变量非条件logistic回归模型估计IL-6和TNF-α水平或基因型(对数加和模型)的比值比(OR)和95%置信区间(95% CI)。与IL-6的最低三分位数相比,调整后的OR为1.06(0.75 - 1.44)和1.01(0.72 - 1.40),分别为第2和第3个三分位数TNF-α的相应OR值分别为0.85(0.63 ~ 1.15)和1.01(0.75 ~ 1.36)(Ptrend = 0.39)。种族分层分析未发现任何显著相关性。IL-6和TNF-α SNPs与结肠腺瘤之间也没有统计学显著性关联。我们的研究结果不支持诊断前IL-6、TNF-α或其遗传变异水平是结肠腺瘤发生的重要危险因素。
Interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α), two important inflammatory cytokines, have been inconsistently associated with risk of colon neoplasia in epidemiological studies. However, research to date has not adequately assessed whether race-specific differences may exist in associations between biomarkers and genetic variants of these cytokines and colorectal adenoma - the precursor lesions of colorectal cancer. We sought to determine whether circulating levels of IL-6 and TNF-α, or genetic polymorphisms in IL-6and TNF-α were associated with colon adenoma and if so, whether that association differed by race. We analyzed the associations of circulating levels and single nucleotide polymorphisms (SNPs) of IL-6 and TNF-α with risk of colon adenomas in a colonoscopy -based case-control study of 401 incident adenoma cases and 1,050 controls. We used multivariate unconditional logistic regression models to estimate the odds ratios (OR) and 95% confidence intervals (95% CI) for levels or genotypes (log additive models) of IL-6 and TNF-α. Compared to the bottom tertile of IL-6, the adjusted ORs were 1.06 (0.75 - 1.44) and 1.01 (0.72 - 1.40), respectively for the 2nd and 3rd tertiles (Ptrend = 0.10); the corresponding ORs for TNF-α were: 0.85 (0.63 - 1.15) and 1.01 (0.75 - 1.36), respectively (Ptrend = 0.39). Race-stratified analyses did not reveal any significant associations. There were also no statistically significant associations between IL-6 and TNF-α SNPs and colon adenoma. Our results do not support pre-diagnostic levels of IL-6, TNF-α or their genetic variants as significant risk factors for the development of colon adenoma.