Zhou Chao, Chen Hao, Wang An
Department of Respiratory Medicine, Zhou Pu Hospital, 135 Guanyue Road, Pudong new District, Shanghai, 201318, China,
Tumour Biol. 2013 Oct;34(5):2961-9. doi: 10.1007/s13277-013-0859-z. Epub 2013 May 30.
The role of p53 codon 72 polymorphism in the development of lung cancer remains obscure due to inconsistent findings of individual case-control studies published to date. A meta-analysis was conducted to better estimate the association between the p53 codon 72 variant and lung cancer risk. All relevant publications from the PubMed, Embase, Web of Science, and Wanfang databases were retrieved. Based on the inclusion criteria, 39 publications involving 44 independent case-control studies were finally included into this meta-analysis. Data were extracted and the pooled odds ratio (OR) with the corresponding 95 % confidence interval (95 % CI) was calculated. The overall pooled ORs showed no significant relationship of the p53 codon 72 polymorphism with increased or decreased risk of lung cancer in all gene contrast models (OR Pro vs. Arg = 1.04, 95 % CI = 0.96-1.13, P OR < 0.001; OR Pro/Pro vs. Arg/Arg = 1.07, 95 % CI = 0.91-1.25, P OR < 0.001; OR Arg/Pro vs. Arg/Arg =1.04, 95 % CI = 0.94-1.15, P OR < 0.001; OR Pro/Pro + Arg/Pro vs. Arg/Arg = 1.04, 95 % CI = 0.94-1.16, P OR < 0.001; OR Pro/Pro vs. Arg/Arg + Arg/Pro = 1.07, 95 % CI = 0.93-1.23, P OR < 0.001). According to the ethnicity, no significant association was observed in subgroup analyses of the Asians, Caucasians, Africans and the mixed population. Similar finding was found in subgroup analyses of hospital-based and population-based studies. Concerning the histological types of lung cancer, the p53 codon 72 variant exerts risk effect on the lung carcinogenesis in patients with adenocarcinoma (OR Arg/Pro vs. Arg/Arg = 1.10, 95 % CI = 1.00-1.22, P OR = 0.048). Additionally, subgroup analysis by the smoking status demonstrated that the p53 codon 72 variant seemed to play a protective role in lung carcinogenesis among the non-smokers but not the smokers in the contrast model of Arg/Pro vs. Arg/Arg (OR Arg/Pro vs. Arg/Arg = 0.71, 95 % CI = 0.50-1.00, P OR = 0.049). The present meta-analysis suggests the p53 codon 72 polymorphism may weakly modify the risk for lung cancer among the adenocarcinoma patients and non-smokers. Nevertheless, this association needs further confirmation in future studies with high quality.
由于迄今为止发表的个别病例对照研究结果不一致，p53密码子72多态性在肺癌发生中的作用仍不清楚。进行了一项荟萃分析，以更好地估计p53密码子72变体与肺癌风险之间的关联。检索了来自PubMed、Embase、Web of Science和万方数据库的所有相关出版物。根据纳入标准，最终将39篇涉及44项独立病例对照研究的出版物纳入本荟萃分析。提取数据并计算合并比值比（OR）及相应的95%置信区间（95%CI）。在所有基因对比模型中，总体合并OR显示p53密码子72多态性与肺癌风险增加或降低均无显著关系（OR Pro vs. Arg = 1.04，95%CI = 0.96 - 1.13，P OR < 0.001；OR Pro/Pro vs. Arg/Arg = 1.07，95%CI = 0.91 - 1.25，P OR < 0.001；OR Arg/Pro vs. Arg/Arg = 1.04，95%CI = 0.94 - 1.15，P OR < 0.001；OR Pro/Pro + Arg/Pro vs. Arg/Arg = 1.04，95%CI = 0.94 - 1.16，P OR < 0.001；OR Pro/Pro vs. Arg/Arg + Arg/Pro = 1.07，95%CI = 0.93 - 1.23，P OR < 0.001）。根据种族，在亚洲人、高加索人、非洲人和混合人群的亚组分析中未观察到显著关联。在基于医院和基于人群的研究的亚组分析中也发现了类似结果。关于肺癌的组织学类型，p53密码子72变体对腺癌患者的肺癌发生有风险影响（OR Arg/Pro vs. Arg/Arg = 1.10，95%CI = 1.00 - 1.22，P OR = 0.048）。此外，按吸烟状态进行的亚组分析表明，在Arg/Pro vs. Arg/Arg对比模型中，p53密码子72变体在非吸烟者的肺癌发生中似乎起保护作用，但在吸烟者中并非如此（OR Arg/Pro vs. Arg/Arg = 0.71，95%CI = 0.50 - 1.00，P OR = 0.049）。本荟萃分析表明，p53密码子72多态性可能会轻微改变腺癌患者和非吸烟者患肺癌的风险。然而，这种关联需要在未来高质量的研究中进一步证实。
