Abstract
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.
Highlights
Received: 17 June 2019Revised: 30 September 2020Accepted: 30 September 2020Accepted Manuscript online: Version of Record published: Cancer poses a major health problem in both developing and developed countries [1,2,3]
The findings did not support an association between Fibroblast growth factor receptor 4 (FGFR4) rs351855 polymorphism and overall cancer susceptibility in heterozygous (OR = 0.97, 95% confidence interval (CI) = 0.87–1.07, P=0.514, AG vs GG), homozygous
The results indicated 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
Summary
Received: 17 June 2019Revised: 30 September 2020Accepted: 30 September 2020Accepted Manuscript online: Version of Record published: Cancer poses a major health problem in both developing and developed countries [1,2,3]. There were approximately 18.1 million new cases and 9.6 million cancer deaths in 2018 [4]. The exact mechanism of cancer development is not clear yet. Mounting evidence have indicated that cancer development and progression is influenced by environmental and genetic factors [3,5,6,7]. The human fibroblast growth factor receptors (FGFRs), a subfamily of cell surface receptor tyrosine kinases (RTKs), consist of four closely related family members (FGFR1–4) [8]. FGFR activation by a various fibroblast growth factors (FGFs) triggers a cascade that leads to the activation of multiple signal transduction pathways, including the Ras/Raf/MapK, PI3K/Akt, STAT, and PLCγ, which can promote cell survival, License 4.0 (CC BY)
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