Departments of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
Neuro Oncol. 2010 May;12(5):444-52. doi: 10.1093/neuonc/nop057. Epub 2010 Feb 5.
Single nucleotide polymorphisms (SNPs) in inflammation-related genes have previously been shown to alter risks of developing various cancers. However, the effects of such SNPs on glioma risk remain unclear. We used a multistrategic approach to elucidate the relationship between glioma risk, asthma/allergies, and 23 literature-based functional SNPs in 11 inflammation genes. Genotyping was conducted on 373 histologically confirmed adult glioma patients and 365 cancer-free controls from the Harris County Brain Tumor Study. Deviations from the Hardy-Weinberg equilibrium were assessed using the chi(2)-test, and Akaike's information criterion was used to determine the best genetic model for each SNP. Odds ratios (ORs) were calculated both for each SNP individually and for grouped analyses, examining the effects of the numbers of adverse alleles on glioma risk in participants with and without asthma. In the single-locus analysis of the 23 examined SNPs, 1 pro-inflammatory and 2 anti-inflammatory gene SNPs were significantly associated with glioma risk (COX2/PTGS2, rs20417 [OR = 1.41]; IL10, rs1800896 [OR = 1.57]; and IL13, rs20541 [OR = 0.39], respectively). When we examined the joint effects of the risk-conferring alleles of these 3 SNPs, we found a significant trend indicating that the risk increases as the number of adverse alleles increase (P = .005). Stratifying by asthma status, we found that this dose-response-like trend of increasing risk is only present among those without asthma/allergies (P < .0001). Our study indicates that polymorphisms in inflammation genes are associated with glioma susceptibility, especially when a history of asthma/allergies is absent.
单核苷酸多态性（SNP）在炎症相关基因中已被证明可以改变各种癌症的发病风险。然而，这些 SNP 对神经胶质瘤风险的影响仍不清楚。我们使用多策略方法阐明了神经胶质瘤风险、哮喘/过敏与 11 个炎症基因中 23 个基于文献的功能 SNP 之间的关系。在哈里斯县脑肿瘤研究中，对 373 例经组织学证实的成年神经胶质瘤患者和 365 例无癌症对照进行了基因分型。使用卡方检验评估 Hardy-Weinberg 平衡偏离情况，Akaike 信息准则用于确定每个 SNP 的最佳遗传模型。分别对每个 SNP 以及分组分析进行了优势比（OR）计算，检查了哮喘患者和非哮喘患者中不利等位基因数量对神经胶质瘤风险的影响。在对 23 个检测 SNP 的单基因座分析中，1 个促炎和 2 个抗炎基因 SNP 与神经胶质瘤风险显著相关（COX2/PTGS2，rs20417[OR=1.41]；IL10，rs1800896[OR=1.57]；和 IL13，rs20541[OR=0.39]）。当我们检查这 3 个 SNP 的风险等位基因的联合效应时，我们发现了一个显著的趋势，表明随着不利等位基因数量的增加，风险增加（P=0.005）。按哮喘状态分层，我们发现这种风险增加的剂量反应样趋势仅存在于无哮喘/过敏的人群中（P<0.0001）。我们的研究表明，炎症基因中的多态性与神经胶质瘤易感性相关，特别是当不存在哮喘/过敏病史时。
