Mandal Raju K, Mittal Rama D
1Research and Scientific Unit, College of Nursing and Allied Health Sciences, Jazan University, Jazan, Kingdom of Saudi Arabia.
2Department of Urology and Renal Transplantation, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, India.
Indian J Clin Biochem. 2020 Jan;35(1):8-19. doi: 10.1007/s12291-018-0787-1. Epub 2018 Sep 17.
involved in the metabolism of carcinogens and toxins, reduces damage of DNA and act as a suppressor of carcinogenesis. Many studies have reported that 313 A > G polymorphism is associated with different cancer in Indian population, but the results remain conflicting rather than conclusive. Therefore, we have performed meta-analysis to clarify the more precise association of 313 A > G polymorphism with cancer risk in Indian population. We retrieved all relevant published literature from PubMed (Medline) and Google scholar web database and included those study only based on the established inclusion criteria. Pooled ORs and 95% CIs were used to appraise the strength of association. Publication bias and sensitivity analysis was also evaluated. A total of 6581 confirmed cancer cases and 8218 controls were included from eligible thirty nine case-controls studies. Pooled analysis suggested that the variant genotypes significantly increased the risk of cancer in allele (G vs. A: OR 1.266, 95% CI 1.129-1.418, = 0.001), heterozygous (AG vs. AA: OR 1.191, 95% CI 1.047-1.355, = 0.008), homozygous (GG vs. AA: OR 1.811, 95% CI 1.428-2.297, = 0.001), dominant (GG + AG vs. AA: OR 1.276, 95% CI 1.110-1.466, = 0.001) and recessive (GG vs. AG + AA: OR 1.638, 95% CI 1.340-2.002, = 0.001) genetic models. The stability of these observations was confirmed by a sensitivity analysis. Begger's funnel plot and Egger's test did not reveal any publication bias. This meta-analysis suggests that the 313 A > G polymorphism may contribute to genetic susceptibility to cancer in Indian population. However, larger studies and randomized clinical trial will be required to elucidate the biological and molecular mechanism of gene in cancer.
参与致癌物和毒素的代谢,减少DNA损伤并起到癌症发生抑制因子的作用。许多研究报告称,313 A > G多态性与印度人群中的不同癌症相关,但结果仍然相互矛盾而非确凿无疑。因此,我们进行了荟萃分析,以阐明313 A > G多态性与印度人群癌症风险之间更精确的关联。我们从PubMed(Medline)和谷歌学术网络数据库中检索了所有相关的已发表文献,并仅根据既定的纳入标准纳入那些研究。合并的比值比(OR)和95%置信区间(CI)用于评估关联强度。还评估了发表偏倚和敏感性分析。从符合条件的39项病例对照研究中纳入了总共6581例确诊癌症病例和8218例对照。汇总分析表明,在等位基因(G vs. A:OR 1.266,95% CI 1.129 - 1.418,P = 0.001)、杂合子(AG vs. AA:OR 1.191,95% CI 1.047 - 1.355,P = 0.008)、纯合子(GG vs. AA:OR 1.811,95% CI 1.428 - 2.297,P = 0.001)、显性(GG + AG vs. AA:OR 1.276,95% CI 1.110 - 1.466,P = 0.001)和隐性(GG vs. AG + AA:OR 1.638,95% CI 1.340 - 2.002,P = 0.001)遗传模型中,变异基因型显著增加了癌症风险。敏感性分析证实了这些观察结果的稳定性。Begger漏斗图和Egger检验未显示任何发表偏倚。这项荟萃分析表明,313 A > G多态性可能导致印度人群对癌症的遗传易感性。然而,需要更大规模的研究和随机临床试验来阐明该基因在癌症中的生物学和分子机制。