Chen Fang-Chun, Zhang Fan, Zhang Zhi-Jiao, Meng Si-Ying, Wang Yang, Xiang Xue-Rong, Wang Chun, Tang Yu-Ying
Department of Oral Medicine, The Affiliated Hospital of Stomatology, Chongqing Medical University; Chongqing Key Laboratory for Oral Diseases and Biomedical Sciences, Chongqing, China E-mail :
Asian Pac J Cancer Prev. 2013;14(12):7243-9. doi: 10.7314/apjcp.2013.14.12.7243.
Numerous studies have been conducted regarding association between TNF-α and oral cancer risk, but the results remain controversial. The present meta-analysis is performed to acquire a more precise estimation of relationships. Databases of Pubmed, the Cochrane library and the China National Knowledge Internet (CNKI) were retrieved until August 10, 2013. Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated with fixed- or random-effect models. The heterogeneity assumption was assessed by I-squared test. Among the eight included case-control studies, all were focused on TNF-α-308G>A and four also concerned the TNF-α-238G>A polymorphism. It was found that oral cancer risk were significant decreased with the TNF-α-308G>A polymorphism in the additive genetic model (GG vs. AA, OR=0.19, 95% CI: [0.04, 1.00], P=0.05, I2=68.9%) and the dominant genetic model (GG+GA vs. AA, OR=0.22, 95% CI: [0.06, 0.82], P=0.03, I2=52.4%); however, no significant association was observed in allele contrast (G vs. A, OR=0.70, 95% CI: [0.23, 2.16], P=0.54, I2=95.9%) and recessive genetic models (GG vs. GA+AA, OR=0.72, 95% CI: [0.33, 1.57], P=0.41, I2=93.1%). For the TNF-α-238G>A polymorphism, significant associations with oral cancer risk were found in the allele contrast (G vs. A, OR=2.75, 95% CI: [1.25, 6.04], P=0.01, I2=0.0%) and recessive genetic models (GG vs. GA+AA, OR=2.23, 95%CI: [1.18, 4.23], P=0.01, I2=0.0%). Conclusively, this meta-analysis indicates that TNF-α polymorphisms may contribute to the risk of oral cancer. Allele G and the GG+GA genotype of TNF-α- 308G>A may decrease the risk of oral cancer, while allele G and the GG genotype of TNF-α-238G>A may cause an increase.
关于肿瘤坏死因子-α（TNF-α）与口腔癌风险之间的关联，已经开展了大量研究，但结果仍存在争议。进行本次荟萃分析是为了更精确地评估二者之间的关系。检索了截至2013年8月10日的PubMed、Cochrane图书馆和中国知网（CNKI）数据库。采用固定效应模型或随机效应模型计算合并比值比（OR）和95%置信区间（95%CI）。通过I²检验评估异质性假设。在纳入的8项病例对照研究中，所有研究均聚焦于TNF-α -308G>A，其中4项研究还涉及TNF-α -238G>A多态性。结果发现，在加性遗传模型（GG与AA相比，OR = 0.19，95%CI：[0.04, 1.00]，P = 0.05，I² = 68.9%）和显性遗传模型（GG + GA与AA相比，OR = 0.22，95%CI：[0.06, 0.82]，P = 0.03，I² = 52.4%）中，TNF-α -308G>A多态性使口腔癌风险显著降低；然而，在等位基因对比（G与A相比，OR = 0.70，95%CI：[0.23, 2.16]，P = 0.54，I² = 95.9%）和隐性遗传模型（GG与GA + AA相比，OR = 0.72，95%CI：[0.33, 1.57]，P = 0.41，I² = 93.1%）中未观察到显著关联。对于TNF-α -238G>A多态性，在等位基因对比（G与A相比，OR = 2.75，95%CI：[1.25, 6.04]，P = 0.01，I² = 0.0%）和隐性遗传模型（GG与GA + AA相比，OR = 2.23，95%CI：[1.18, 4.23]，P = 0.01，I² = 0.0%）中发现与口腔癌风险存在显著关联。总之，本次荟萃分析表明，TNF-α多态性可能与口腔癌风险有关。TNF-α -308G>A的等位基因G以及GG + GA基因型可能降低口腔癌风险，而TNF-α -238G>A的等位基因G以及GG基因型可能增加口腔癌风险。
