ASSOCIATION BETWEEN APE1 ASP148GLU AND COLORECTAL CANCER RISK: A META-ANALYSIS

ASSOCIATION BETWEEN APE1 ASP148GLU AND COLORECTAL CANCER RISK: A META-ANALYSIS
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APE1 ASP148GLU 与结直肠癌风险之间的关联:荟萃分析。

DOI:
10.25011/cim.v43i4.34987
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发表时间:
2020-12-01
影响因子:
0.8
通讯作者:
Wang,Weibing
Wang,Weibing
中科院分区:
医学4区
文献类型:
--
作者:
Lin,Caizhao;Jin,Yuewei;Wang,Weibing

文献摘要

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背景 结直肠癌(CRC)是全球公认的最常见的癌症之一。CRC与脱嘌呤核酸内切酶1(APE 1)Asp 148 Glu多态性之间的关联尚不清楚;因此,本荟萃分析旨在探讨APE 1 Asp 148 Glu多态性是否与CRC风险相关。 方法 系统检索Embase、PubMed、科克伦图书馆、CNKI和万方数据库,直至2020年4月17日,以评价APE 1 Asp 148 Glu多态性对CRC风险的影响。用Asp 148 Glu多态性与结直肠癌风险之间的比值比(OR)和95%置信区间(CI)评估相关强度。还进行了亚组分析。 结果 共纳入11篇文章,包括8,136例受试者(3,836例病例和4,300例对照)。分析了5种遗传模型,包括加性模型(G vs. T)、杂合子比较(TG vs. TT)、纯合子比较(GG vs. TT)、显性模型(TG+GG vs. TT)和隐性模型(GG vs. TG+TT)。在这些模型中,T是指胸腺嘧啶,G是指鸟嘌呤。APE 1 Asp 148 Glu多态性在杂合子比较[OR(95%CI)= 1.36(1.05,1.75),P=0.019]和显性模式[OR(95%CI)=1.31(1.07,1.61),P=0.010]中显著增加了结直肠癌的风险。在加性模型[OR(95%CI)= 1.14(1.00,1.31),P=0.057]、隐性模型[OR(95%CI)= 0.97(0.71,1.31),P=0.826]或纯合子比较[OR(95%CI)= 1.15(0.88,1.52),P=0.309]中未观察到显著相关性。APE 1 Asp 148 Glu基因多态性与结直肠癌的危险性存在显著相关性,在PCR-RFLP加性模型、纯合子比较和隐性模型(PG)中,APE 1 Asp 148 Glu基因多态性可能是结直肠癌的潜在危险因素。
BACKGROUND Colorectal cancer (CRC) is recognized as one of the most common cancer globally. The association between CRC and apurinic endonuclease 1 (APE1) Asp148Glu polymorphism remains unclear; thus, this meta-analysis aimed to explore whether APE1 Asp148Glu polymorphism is related to CRC risk. METHODS Embase, PubMed, Cochrane library, CNKI and Wanfang databases were subject to a systematic search until April, 17, 2020 to evaluate the effect of APE1 Asp148Glu polymorphism on CRC risk. The associated strength was used to evaluate with odds ratios (ORs) with 95% confidence intervals (CIs) between Asp148Glu polymorphism and CRC risk. Subgroup analyses were also performed. RESULTS In total, 11 articles including 8,136 subjects (3,836 cases and 4,300 controls) were included. Five genetic models were analyzed, including the additive model (G vs. T), the heterozygote comparison (TG vs. TT), the homozygote comparison (GG vs. TT), the dominant model (TG+GG vs. TT), and the recessive model (GG vs. TG+TT). In these models, T refers to thymine and G refers to guanine. The APE1 Asp148Glu polymorphism in heterozygote comparison [OR (95%CI) = 1.36 (1.05, 1.75), P=0.019] and dominant model [OR (95%CI) =1.31 (1.07, 1.61), P=0.010] significantly increased CRC risk. No significant association was seen for the additive model [OR (95%CI) = 1.14 (1.00, 1.31), P=0.057], recessive model [OR (95%CI) = 0.97 (0.71, 1.31), P=0.826] or in homozygote comparison [OR (95%CI) = 1.15 (0.88, 1.52), P=0.309]. Moreover, CRC risk indicated a remarkable association with APE1 Asp148Glu polymorphism in the PCR-RFLP additive model, homozygote comparison and recessive model (PG) may be a potential risk factor for CRC.