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Objective To identify the potential long non-coding RNA (lncRNA) expressed in rheumatoid arthritis (RA) synovium key to RA onset and investigate its association with immune cell infiltration. Methods RA synovium data were downloaded from the GEO database and normalized. The lncRNAs key to RA onset were identified using multiple machine learning methods. Infiltration of 22 immune cell populations in RA synovium was measured by cell-type identification by estimating relative subsets of RNA transcripts (CIBER-SORT). The relationship between the key lncRNA and infiltrating immune cells was analyzed. Finally, real-time quantitative PCR was applied to validate the expression of the key lncRNA in RA synovial cells. Results lncRNA human leukocyte antigen complex P5(HCP5) was identified as the key lncRNA associated with RA onset. Infiltration analysis revealed increased abundance of CD8 + T cells, γδ T cells, and M1 macrophages while decreased abundance of M2 macrophages in RA synovial tissue. Correlation analysis demonstrated that the lncRNA HCP5 expression was positively associated with the infiltration abundance of CD8 + T cells, γδ T cells, and M1 macrophages in RA synovial tissue. Furthermore,the expression of lncRNA HCP5 in RA synovial cells was up-regulated. Conclusion lncRNA HCP5 expression is up-regulated in RA synovial tissue and potentially associated with immune cells infiltration.

Background: Cytochrome P450A1 (CYP1A1) gene and glutathione S-transferase M1 (GSTM1) gene both have single nucleotide polymorphisms and effects on lung cancer. Currently, however, the risk of lung cancer due to the CYP1A1 and GSTM1 genes has no clear evidence. In this present study, we propose to research the combined effects of CYP1A1 gene and GSTM1 gene polymorphism and their risks to lung cancer., Methods: We conducted the study at different research areas and using various database, including PubMed, Embase, China Biology Medicine (CBM) and China National Knowledge Infrastructure (CNKI) last March 31, 2011. We calculated the adjusted odds ratio (OR) and 95% confidence interval (CI) for lung cancer in each study. Using STATA 10, a statistical program, we summarized the calculated estimates for the adjusted ORs and performed a meta-analysis., Results: The meta-analysis includes 15 research studies. The CYP1A1 IIe/Val genotype which carries a homozygous mutant type has a higher chance of risk to lung cancer than that which carries a homozygous mutant type and a heterozygous type when the GSTM1 carries a null genotype. As a result, OR was 3.18 (95%CI: 1.27-7.98), 1.45 (95%CI: 1.08-1.94), respectively. Meanwhile, the same conclusion was obtained for the CYP1A1 MspI genotype. The overall OR was 1.90 (95%CI: 1.00-3.58), 1.57 (95%CI: 1.23-2.00), respectively., Conclusions: We discovered through our meta-analysis that the combined effects of CYP1A1 gene and GSTM1 gene polymorphism are significantly associated with an increased risk to lung cancer. We also found that homozygous mutant genotype of CYP1A1 has a higher chance of risk to lung cancer than the homozygous or heterozygous genotype.

Background: Many studies concluded that the polymorphisms of XPD were involved in the risk of lung cancer. However, several other studies suggested no association. To explore whether the polymorphisms of XPD contribute to the genetic susceptibility to lung cancer, we carried a meta-analysis based on the published works., Methods: All works related to XPD and lung cancer risk were searched and carefully selected. The genotype frequencies of XPD and related variables were abstracted and the pooled ORs were calculated after the heterogeneity test with the software Stata 10. Publication bias and sensitivity were evaluated at the same time., Results: Twenty-two studies were included according to the selection criteria, of which fifteen investigated the codon 312 of XPD and twenty studied the codon 751. The pooled OR of susceptibility to lung cancer with XPD312 Asn/Asn genotype compared to the wild Asp/Asp were 1.18 (95%CI: 1.03-1.34, P=0.018). And the polymorphisms of XPD codon 751 were also associated with increased lung cancer risk (Lys/Gln OR=1.09, 95%CI: 1.02-1.18; Gln/Gln OR=1.24, 95%CI: 1.10-1.41). However, subgroup analysis indicated that the association between XPD751 and lung cancer could only be found in Europeans and Americans. The publication bias analysis had no statistically significant results., Conclusions: Polymorphisms of XPD codons 312 and 751 seem to be involved in elevated risk of lung cancer.

Background: Xeroderma pigmentosum group D (XPD) is one of the important DNA repair genes. XPD polymorphism at Lys751Gln site has been shown to alter XPD protein function, modulate DNA repair capacity and therefore affect cancer risk. The aim of this study is to explore the relationship between XPD polymorphism and susceptibility to lung cancer in nonsmoking female via a population-based case-control study., Methods: There were 105 female patients who were diagnosed with lung cancer between January 2004 and December 2005 from Liaoning Tumor Hospital and 202 Hospital, and the control group included 105 healthy volunteers who were obtained from community centers at the same time. Information concerning demographic and risk factors was obtained for each case and control by a trained interviewer. XPD genotypes of cases and controls were determined by PCR-RFLP method. Two-sided Chi-Square test was used to compare the distribution of the genotypes and risk factors between cases and controls. Unconditional logistic regression analysis was performed to calculate the odds ratios (OR) with 95% confidence intervals (CI) for estimating the association between certain genotypes and lung cancer and exploring the interaction of environmental risk factors and genetic polymorphism., Results: All of the subjects in this study were nonsmoking females in Shenyang. There was no significant demographic difference (age, economic level and education) between cases and controls. There was a significant difference in the frequencies of XPD polymorphism between cancer cases and controls. The frequencies of XPD 751Gln allele were 6.2% in controls and 13.8% in cases (P < 0.05). The risk of lung cancer was higher in those with the Lys/Gln or Gln/Gln genotype than in those with the Lys/Lys genotype and adjusted OR was 2.80 (95% CI: 1.21-6.48). The result showed that cooking fumes exposure was a risk factor for lung cancer (OR was 2.44). Furthermore, an interaction between environmental risk factors and the variant XPD 751Gln allele on the risk of lung cancer was observed. Individuals with both risk gen-otype and exposure to cooking fumes had a higher elevated risk of cancer than those with only one of them (adjusted OR= 6.85 ; 95% CI: 1.69-27.67; P=0.007)., Conclusions: The above findings indicate that the Lys751Gln polymorphism in XPD gene is associated with the risk of lung cancer in nonsmoking females. Individuals with both XPD 751Gln allele genotype and exposure to cooking fumes have a higher elevated risk of cancer than those with only one of them in nonsmoking female population.

Background: XRCC1 polymorphism at Arg399Gln site has been shown to modulate DNA repair capacity. The aim of this study is to assess the relationship between XRCC1 polymorphism and susceptibility to lung adenocarcinoma in nonsmoking female via a hospital-based case-control study., Methods: Cases were 126 female patients with lung adenocarcinoma from January 2002 to October 2004 in China Medical University Hospital and Liaoning Tumor Hospital. Controls were selected from patients with other pulmonary diseases in the hospitals at the same time. These controls were matched to cases on age (±5 years). Information concerning demographic and risk factors was obtained for each case and control by a trained interviewer. XRCC1 genotypes were determined by PCR-RFLP. The adjusted odds ratio (OR) and 95% confidence interval (CI) were calculated using logistic regression., Results: Cases showed a higher prevalence of oil smoke compared with controls (P < 0.05). The frequencies of Arg/Arg, Arg/Gln and Gln/Gln in lung adenocarcinoma group (32.54%, 42.86%, 24.60%) were significantly different from those in controls (54.76%, 40.48%, 4.76%) (P < 0.05). The individual carrying Gln/Gln genotype was at a significantly increased risk of lung adenocarcinoma compared with those with Arg/Arg genotype (OR=8.695, 95%CI 3.343-22.614, adjusted for age and oil smoke exposure). Furthermore, the OR of lung adenocarcinoma for the variant XRCC1 399Gln allele combined with exposure to oil smoke was 5.21 (95%CI 1.85-14.70, P < 0.001)., Conclusions: The results indicate that the Arg399Gln polymorphism in XRCC1 is associated with the risk of lung adenocarcinoma in nonsmoking women.