Background Cytochrome P450 (CYPs) are heme proteins involved in the metabolism of a variety of endogenous and exogenous substances and play an important role in the carcinogenesis mechanisms of environmental and hereditary factors. The objective of this study was to investigate how polymorphisms of CYPs correlate with lung cancer (LC) susceptibility. Methods Six single nucleotide polymorphisms (SNPs) were genotyped in this study. The chi‐square test and unconditional logistic regression model were used to evaluate the correlation between SNPs and LC susceptibility. The expressions and survival data of genes in patients with LC were mined using Oncomine and Kaplan‐Meier Plotter database. Results Four SNPs were found to be significantly associated with the risk of LC development ( P < 0.05). The most significant correlation was that the A allele and AA genotype of CYP2D6 rs1065852 were associated with increased risk of LC development (adjusted odds ratio [OR] = 1.35, 95% confidence interval [95%CI] = 1.13‐1.60, P = 9.04e‐4; OR = 1.83, 95%CI = 1.29‐2.59, P = 0.001 respectively). Similar association of this variant was also found in the subgroups of male patients, cases in III‐IV stages, positive lymph node, squamous cell carcinomas and adenocarcinomas. Whereas rs1065852 was considered as protective factor in females (adjusted OR = 0.33, 95% CI = 0.16‐0.70, P = 0.004). In stratified analyses, the association of CYP24A1 rs2762934, CYP24A1 rs6068816, CYP20A1 rs2043449 polymorphism with LC risk appeared stronger in some subgroups. CYP2D6 , CYP24A1 and CYP20A 1 are overexpressed in some pathological types of LC ( P < 0.05), and high levels of CYP2D6 and CYP20A1 indicate poor and good prognosis of LC, respectively. Conclusion This study revealed that rs1065852, rs2043449, rs2762s934, and rs6068816 of CYPs were associated with LC susceptibility in the Northwestern Chinese Han population; CYP2D6 and CYP20A 1 were overexpressed and correlated with prognosis of LC.

MicroRNAs (miRNAs) are key regulators of gene expression; however, the extent to which single nucleotide polymorphisms (SNPs) interfere with miRNA gene regulation and affect cervical cancer (CC) susceptibility remains largely unknown. Here, we systematically analyzed miRNA-related SNPs and their association with CC risk, and performed a case-control study of miR-17-5p SNPs and CC risk in a Chinese population. Sixteen SNPs were genotyped in 247 CC cases and 285 controls. Three were associated with CC risk (p < 0.05): the minor allele (A) of rs217727 in H19 increased risk (OR = 1.53, p = 0.002), while the minor alleles (T) of rs9931702 and (T) of rs9302648 in AKTIP decreased CC risk (p = 0.018, p = 0.014). Analysis of the SNPs after stratification based on CC clinical stage and subtype revealed that rs1048512, rs6659346, rs217727, rs9931702, and rs9302648 were associated with CC risk in clinical stages I-II; rs2862833, rs2732044, rs1030389, and rs1045935 were associated with CC risk in clinical stages III-IV; and rs217727, rs9931702, and rs9302648 were associated with CC risk in squamous carcinomas. These data could serve as a useful resource for understanding the miR-17 function, identification of miRNAs associated with CC, and development of better CC screening strategies.

Common variants of multiple genes play a role in glioma onset. However, research related to astrocytoma, the most common primary brain neoplasm, is rare. In this study, we chose 21 tagging SNPs (tSNPs), previously reported to be associated with glioma risk in a Chinese case-control study from Xi'an, China, and identified their contributions to astrocytoma susceptibility. We found an association with astrocytoma susceptibility for two tSNPs (rs6010620 and rs2853676) in two different genes: regulator of telomere elongation helicase 1 (RTEL1) and telomerase reverse transcriptase (TERT), respectively. We confirmed our results using recessive, dominant, and additive models. In the recessive model, we found two tSNPs (rs2297440 and rs6010620) associated with increased astrocytoma risk. In the dominant model, we found that rs2853676 was associated with increased astrocytoma risk. In the additive model, all three tSNPs (rs2297440, rs2853676, and rs6010620) were associated with increased astrocytoma risk. Our results demonstrate, for the first time, the potential roles of RTEL1 and TERT in astrocytoma development.

The Epidermal Growth Factor Receptor gene has been reported to be involved in the progression of gliomas which is one of the deadliest primary brain tumors in humans. To determine potential association between EGFR and glioma risk, we performed a case-control study with 394 glioma patients and 298 cancer-free controls in which captured a total of 8 tag single nucleotide polymorphisms of EGFR gene from Xi’an, China. SPSS 19.0 statistical packages, χ2 test, genetic model analysis and SHEsis software platform were analyzed s the variants in EGFR gene associations with glioma risk. For five different inheritance models analyzed, the following genotypes were associated with increased glioma risk. In the codominant model, genotype CC (rs730437, OR = 1.93, p = 0.024; rs1468727, OR = 2.02, p = 0.007); In the dominant model, genotype CA and CC (rs730437, OR = 1.45, p = 0.026), genotype GA and AA (rs845552, OR = 1.40, p = 0.044); In the recessive model, genotype CC (rs730437, OR = 1.64, p = 0.026; rs1468727, OR = 1.87, p = 0.002); In the additive model, genotype CC (rs730437, OR = 1.32, p = 0.006; rs1468727, OR = 1.39, p = 0.005), genotype GG (rs11506105, OR = 1.32, p = 0.02) and genotype AA (rs845552, OR = 1.27, p = 0.04). Our study indicated that 8 mutants located in EGFR gene were risk-conferring factors, larger and different populations with EGFR polymorphisms are required to verify these associations.

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