Abstract
Published data on the association between 8q24 polymorphism and breast cancer (BC) risk are inconclusive. Thus, we conducted a meta-analysis to evaluate the relationship between 8q24 (rs13281615 and rs6983267) polymorphism and BC risk. We searched PubMed, EMBASE, Web of Science and the Cochrane Library up to August 13, 2015 for relevant studies. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to estimate the strength of associations. Twenty-six studies published from 2008 to 2014, with a total of 52,683 cases and 64,672 controls, were included in this meta-analysis. The pooled results showed that there was significant association between 8q24 rs13281615 polymorphism and BC risk in any genetic model. In the subgroup analysis by ethnicity, the effects remained in Asians and Caucasians. However, no genetic models reached statistical association in Africans. There was no association in any genetic model in rs6983267. This meta-analysis suggests that 8q24 rs13281615 polymorphism is a risk factor for susceptibility to BC in Asians, Caucasians and in overall population, While, there was no association in Africans. The rs6983267 polymorphism has no association with BC risk in any genetic model. Further large scale multicenter epidemiological studies are warranted to confirm this finding.
Highlights
There was no association in any genetic model in rs6983267
This meta-analysis suggests that 8q24 rs13281615 polymorphism is a risk factor for susceptibility to Breast cancer (BC) in Asians, Caucasians and in overall population, While, there was no association in Africans
BC-associated gene loci have been demonstrated by GWAS, 8q24 is the gene mutation site selected by this technique [7]
Summary
Lower external rate polymorphism genes [7, 8]. The distribution of these genes in the population is more than 1%, and the genetic variation of these genes (Single nucleotide polymorphism, SNP) is mainly by changing the expression level and function of the protein and the modified factor inside and outside the cell, affecting the genetic susceptibility of BC [8]. Epidemiology and basic etiology studies have shown that BC’s occurrence and progression is closely related to multiple factors interaction between genetic, endocrine and external environment [4,5,6]. The genetic markers of BC are mainly expressed in two forms, that is, the higher external rate mutation gene and the lower external rate polymorphism gene. HWE: Hardy-Weinberg equilibrium; PB: population based; HB: hospital-based; SNP: single nucleotide polymorphism
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