Abstract
Single nucleotide polymorphisms (SNPs) in the telomere-associated gene ACYP2 are associated with increased lung cancer risk. We explored the correlation between ACYP2 SNPs and lung cancer susceptibility in the Chinese Han population. A total of 554 lung cancer patients and 603 healthy controls were included in this study. Thirteen SNPs in ACYP2 were selected. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated using unconditional logistic regression analysis. Multivariate logistic regression analysis was used assess the correlation between SNPs and lung cancer. We found that rs1682111 was associated with increased lung cancer risk in the recessive model (crude, OR=1.50, 95%CI: 1.04-2.16, p=0.029; adjusted for age, OR=1.55, 95%CI: 1.04-2.30, p=0.029), as was rs11896604 in the codominant model (crude, OR=0.65, 95%CI: 0.33-1.28, p=0.045; adjusted for age, OR=0.74, 95%CI: 0.36-1.53, p=0.049) and over-dominant model (crude, OR=1.30, 95%CI: 1.02-1.66, p=0.032; adjusted for age, OR=1.37, 95%CI: 1.05-1.78, p=0.020). Finally, rs843720 was associated with increased lung cancer risk in the recessive model (crude, OR=1.43, 95%CI: 1.02-2.02, p=0.040; adjusted for age, OR=1.48, 95%CI: 1.02-2.15, p=0.040). Thus three SNPs in ACYP2 (rs1682111, rs11896604 and rs843720) associate with lung cancer in the Chinese Han population.
Highlights
Lung cancer, the leading cause of cancer-related death in most countries, has been increasing rapidly in China for the last three decades [1]
We explored the correlation between ACYP2 single nucleotide polymorphisms (SNPs) and lung cancer susceptibility in the Chinese Han population
Comparing the differences in the frequency distributions of the alleles between the cases and controls using the χ2 test, we found no correlation between the loci and lung cancer susceptibility
Summary
The leading cause of cancer-related death in most countries, has been increasing rapidly in China for the last three decades [1]. The risk of lung cancer is strongly associated with exposure to environmental carcinogens, in particular to cigarette smoke [2]. Only approximately 10% of smokers ever develop lung cancer. This highlights the potential role of hereditary components in determining the risk of lung cancer [3]. Through genome-wide association studies (GWAS), a number of genes involved in lung carcinogenesis have been identified in populations of European descent. These include CHRNA5, CHRNA3 and CHRNA4 on chromosome 15q25.1 [4,5,6], (TERT-CLPTM1L) on 5p15.33 [7, 8], and (BAT3-MSH5) on 6p21.33 [7]
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