Abstract
Published data on the association between PRKAA1 rs13361707 T > C polymorphism and gastric cancer (GCa) susceptibility were inconclusive. To derive a more precise estimation of the association, we conducted a large-scale GCa study of 1,124 cases and 1,194 controls to confirm this association in an eastern Chinese population. Our results showed that the C allele of PRKAA1 rs13361707 increased the GC risk in the study population [CT vs. TT, odds ratio (OR) = 1.72, 95% confidence interval (CI) = 1.40-2.12; CC vs. TT, OR = 2.15, 95%CI = 1.70-2.71; CT/CC vs. TT, OR = 1.86, 95%CI = 1.53-2.26; CC vs.TT/CT, OR = 1.49, 95%CI = 1.24-1.79]. In addition, the association of C allele with an increased GCa risk was still significant in subgroups, when stratified by age, sex, tumor site, drinking and smoking status. Moreover, the findings in the present study were validated by our further meta-analysis. In summary, these results indicated that the C allele of PRKAA1 rs13361707 was a low-penetrate risk factor for GCa.
Highlights
Gastric cancer (GCa) is currently the most frequently occurring cancer and one of the leading causes of cancer-related death in the world
The results indicated that the C allele of PRKAA1 rs13361707 increases GC risk[CT vs. TT, odds ratio (OR) = 1.72, 95% confidence interval (CI) = 1.40–2.12; CC vs. TT, OR = 2.15, 95%CI = 1.70–2.71; CT/CC vs. TT, OR = 1.86, 95%CI = 1.53–2.26; CC vs.TT/CT, OR = 1.49, 95%CI = 1.24–1.79; and additive model, OR = 1.46, 95%CI = 1.30– 1.64] in the study population
Apart from environmental and lifestyle factors for GCa risk, genetic factors in the GCa development were important in identifying at-risk populations for cancer prevention
Summary
Gastric cancer (GCa) is currently the most frequently occurring cancer and one of the leading causes of cancer-related death in the world. A total of 951,600 new GCa cases and 723,100 deaths are estimated to have occurred in 2012, accounting for 8% of the total cases and 10% of total deaths [1]. Mechanism of gastric carcinogenesis is still not fully understood, it has been suggested that environmental factors combining with low-penetrance susceptibility genes may be important. Because only few HP carriers eventually develop GCa, other factors must play a role in GCa risk. Life styles, such as tobacco smoking and diet, are suggested as potential risk factors for www.impactjournals.com/oncotarget
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