Tropical and Communicable Diseases Research Centre, Iranshahr University of Medical Sciences, Iranshahr, Iran.
Department of Clinical Biochemistry, Iranshahr University of Medical Sciences, Iranshahr, Iran.
Biosci Rep. 2020 Oct 30;40(10). doi: 10.1042/BSR20192051.
Fibroblast growth factor receptor 4 (FGFR4) is a cell surface receptor tyrosine kinases (RTKs) for FGFs. Several studies have focused on the association between FGFR4 polymorphisms and cancer development. This meta-analysis aimed to estimate the association between FGFR4 rs351855 (Gly388Arg), rs1966265 (Val10Ile), rs7708357, rs2011077, and rs376618 polymorphisms and cancer risk. Eligible studies were identified from electronic databases. All statistical analyses were achieved with the STATA 14.0 software. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were used to quantitatively estimate the association. Overall, no significant association was found among rs351855, rs2011077, and rs376618 polymorphisms with the risk of overall cancer. The rs1966265 polymorphism significantly decreased the risk of cancer in recessive (OR = 0.87, 95% CI = 0.78-0.97, P=0.009, TT vs CT+CC) genetic model. Whereas the rs7708357 polymorphism was positively associated with cancer risk in dominant (OR = 1.17, 95% CI = 1.02-1.36, P=0.028) genetic model. Stratified analysis revealed that rs351855 variant significantly increased the risk of prostate cancer in heterozygous (OR = 1.16, 95% CI = 1.02-1.32, P=0.025 AG vs GG), dominant (OR = 1.20, 95% CI = 1.06-1.35, P=0.004, AG+AA vs GG), and allele (OR = 1.22, 95% CI = 1.06-1.41, P=0.005, A vs G) genetic models. In summary, the findings of this meta-analysis indicate that rs1966265, rs7708357, and rs351855 polymorphisms are correlated to cancer development. Further well-designed studies are necessary to draw more precise conclusions.
成纤维细胞生长因子受体 4(FGFR4)是细胞表面受体酪氨酸激酶(RTKs),可与成纤维细胞生长因子(FGFs)结合。多项研究集中于 FGFR4 多态性与癌症发展之间的关系。本荟萃分析旨在评估 FGFR4 rs351855(Gly388Arg)、rs1966265(Val10Ile)、rs7708357、rs2011077 和 rs376618 多态性与癌症风险之间的关系。从电子数据库中确定了符合条件的研究。所有统计分析均使用 STATA 14.0 软件进行。使用 95%置信区间(CI)的合并优势比(OR)定量评估关联。总体而言,rs351855、rs2011077 和 rs376618 多态性与总体癌症风险之间无显著相关性。rs1966265 多态性在隐性遗传模型(OR=0.87,95%CI=0.78-0.97,P=0.009,TT 与 CT+CC)中显著降低了癌症风险。而 rs7708357 多态性在显性遗传模型(OR=1.17,95%CI=1.02-1.36,P=0.028)中与癌症风险呈正相关。分层分析显示,rs351855 变体在杂合子(OR=1.16,95%CI=1.02-1.32,P=0.025,AG 与 GG)、显性(OR=1.20,95%CI=1.06-1.35,P=0.004,AG+AA 与 GG)和等位基因(OR=1.22,95%CI=1.06-1.41,P=0.005,A 与 G)遗传模型中显著增加了前列腺癌的风险。总之,本荟萃分析的结果表明,rs1966265、rs7708357 和 rs351855 多态性与癌症发展有关。需要进一步设计良好的研究来得出更准确的结论。