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Investigation of leptin receptor rs1137101 GA polymorphism with cancer risk: evidence from 35936 subjects

机译:瘦素受体rs1137101 G A多态性与癌症风险的关系研究:来自35936名受试者的证据

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摘要

Leptin receptor (LEPR) signaling may be involved in promoting angiogenesis and proliferation, inhibiting apoptosis and playing a vital role in the progression of carcinogenesis. A number of studies have focused on the association of LEPR rs1137101 variants with susceptibility of cancer, however, the observed results were controversial. We searched literature on the relationship of LEPR rs1137101 G>A polymorphism with cancer risk by using PubMed and Embase databases, covering all publications up to 14 October 2018. In total, 44 case–control studies with 35,936 subjects were included. After combining all eligible studies, we identified null relationship between LEPR gene rs1137101 G>A polymorphism and overall cancer risk [A vs. G: odds ratio (OR ) =  0.97, 95% confidence interval (CI ) =  0.89–1.06, P = 0.547; AA vs. GG: OR  =  0.93, 95% CI  =  0.78–1.13, P = 0.476; AA/GA vs. GG: OR  =  0.99, 95% CI  =  0.91–1.09, P= 0.890 and AA vs. GA/GG: OR  = 0.92, 95% CI  =  0.82–1.04, P= 0.198]. However, in a subgroup analysis, there was an increased susceptibility of oral and oropharyngeal cancer in AA vs. GA/GG genetic model (OR, 1.83; 95% CI, 1.01–3.33; P=0.048). Considering the limited participants were included, the findings might be underpowered. Sensitivity analysis identified that any independent study omitted did not materially influence the pooled ORs and CIs. The results of publication bias detection showed that there was no evidence of bias. In summary, this analysis indicates that no significant association of cancer risk was identified to be correlated with rs1137101 G>A variants, even in stratified analyses.
机译:瘦素受体(LEPR)信号可能参与促进血管生成和增殖,抑制细胞凋亡,并在致癌过程中发挥重要作用。许多研究集中在LEPR rs1137101变异与癌症易感性的关系上,但是,观察到的结果存在争议。我们使用PubMed和Embase数据库搜索了有关LEPR rs1137101 G> A多态性与癌症风险之间关系的文献,涵盖了截至2018年10月14日的所有出版物。总共包括44个病例对照研究,涉及35,936名受试者。合并所有符合条件的研究后,我们确定了LEPR基因rs1137101 G> A多态性与总体癌症风险之间没有无效关系[A vs. G:优势比(OR)= 0.97,95%置信区间(CI)= 0.89–1.06,P = 0.547; AA vs. GG:OR = 0.93,95%CI = 0.78-1.13,P = 0.476; AA / GA与GG:OR = 0.99,95%CI = 0.91-1.09,P = 0.890,而AA与GA / GG:OR 0.9 = 0.92,95%CI = 20.82-1.04,P = 0.198]。然而,在亚组分析中,AA和GA / GG遗传模型相比,口腔癌和口咽癌的易感性增加(OR,1.83; 95%CI,1.01-3.33; P = 0.048)。考虑到包括有限的参与者,结果可能没有足够的动力。敏感性分析表明,任何独立研究都没有对合并的OR和CI产生实质性影响。出版偏差检测的结果表明,没有证据表明存在偏差。总之,该分析表明,即使在分层分析中,也未发现与rs1137101 G> A变体相关的癌症风险显着相关。

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