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This study investigates the extraction of vanadium from low-vanadium grade magnetite concentrate pellets using sodium salt. 71.1% of vanadium can be extracted under the following optimal conditions: pelletizing with 5 wt% Na2CO3, preheating at 1050 °C for 10 min, roasting at 1250 °C for 10 min, and water leaching at 120 °C for 120 min with a liquid:solid ratio of 5:1 (mL/g) in the bench-scale experiment. XPS and SEM-EDS results showed that part of trivalent vanadium was not oxidized completely during the sodium salt roasting and still occurred in the iron mineral phase; consequently, this part of vanadium was retained in the leached iron ore. The sodium salt roasting parameters are consistent with those of the iron ore oxidized pellets produced by grate-kiln or straight-grate methods; thus, the production efficiency of sodium salt roasting for vanadium extraction can be improved significantly. Pilot-scale experiment was further performed to verify the feasibility of the recommended method in a traveling grate, a better vanadium extraction ratio of 79.1% was achieved.

To investigate the association between smoking, environmental tobacco smoke (ETS), and lung cancer risk. This case–control study included 1622 newly diagnosed cases of lung cancer and 1622 healthy frequency-, age-, and gender-matched control participants. Epidemiological data were collected by in-person interviews using a standard questionnaire. Smoking was a risk factor for lung cancer in men (odds ratio (OR) = 4.486, 95% confidence interval (95%CI) 3.586–5.611). In addition, decreased starting age, increased number of cigarettes smoked per day, duration of smoking, pack–years, and depth of inhalation were all risk factors that met the dose–response relationship (P

Long noncoding RNAs (lncRNAs) dysregulation leads to malignant progression of lung cancer. Our study profiled differentially expressed lncRNA and mRNA in tumor and normal tissues of lung adenocarcinoma (LUAD). Further, analysis of the gene expression profiles of LUAD tissues (n = 533) and normal tissues (n = 59) from The Cancer Genome Atlas (TCGA). A total of 138 lncRNAs were differentially expressed between LUAD tissues and normal tissues (false discovery rate [FDR] q, We performed a study in 8 lung adenocarcinomas patients and validated our observations using The Cancer Genome Atlas (TCGA) dataset. We found that 138 lncRNAs were upregulated or down regulated similarly to those in our microarray study. The lncRNA–mRNA co‐expression network was constructed based on the correlation analysis. Our results revealed that the lncRNA A2M‐AS1 exhibited the highest correlation with the co‐expressed mRNAs, indicating that it might play a key role in regulating differential gene expression in lung adenocarcinomas patients.

BACKGROUND To investigate whether human papillomavirus (HPV) infection is associated with primary lung cancer among the Fujian population. METHODS HPV infection was detected in 140 pairs of lung cancer tissues and matched paracancerous tissues by examining the 21 clinically relevant HPV types using a combination of viral highly conserved L1 region PCR amplification and specific probe reverse hybridization. Paired χ2 test was used to analyze differences in detection rates of HPV between lung cancer and paracancerous tissues. Differences in detection rates of HPV in lung cancer tissues were analyzed using χ2 test or the exact probability method. The rank sum test was used to analyze differences in the distributions of routine indices of blood and pulmonary function in lung cancer tissues between the HPV negative and positive groups. RESULTS HPV infection was detected in 13 of the 140 tumor specimens and in 16 of the paired normal lung tissues. There was no significant correlation between HPV infection and lung cancer (P > 0.05). The diagnosed HPV infection rates did not differ significantly among lung cancer tissues with different stratification (P > 0.05). However, the platelet count, platelet pressure, residual gas volume, functional residual volume, and residual gas volume/lung total distribution may differ between HPV-negative and HPV-positive lung cancer tissues (0.000625 < P

Objective In this study, we analyzed the association between genetic variants of genes in the NOTCH signaling pathway and the prognosis of non-small-cell lung cancer (NSCLC) in the Chinese population. We also explored the interaction between genetic and epidemiological factors for the test group. Methods We performed genotyping of 987 NSCLC patients. Then, we used Cox proportional hazard models to analyze the associations between single-nucleotide polymorphisms (SNPs) and the prognosis of NSCLC. We employed Stata software to test the heterogeneity of associations between subgroups, and we analyzed the additive and multiplicative interactions between SNPs and epidemiologic factors. Results This work revealed the important prognostic and predictive value of rs915894 in the NOTCH4 gene, which may be regarded as a promising prognosis biomarker of NSCLC. Cox regression analysis indicated that the C allele of rs915894 is associated with longer survival and decreased risk of death in NSCLC (codominant model: adjusted HR =0.83, 95% CI =0.70-0.99; dominant model: adjusted HR =0.83, 95% CI =0.71-0.98). Additional stepwise regression analysis suggested that this SNP is an independently favorable factor for the prognosis of NSCLC (dominant model: adjusted HR =0.85, 95% CI =0.72-0.99). This protective effect is more pronounced for patients who are not smokers, have a history of other lung diseases, or have a family history of cancer. We also detected statistically significant additive and multiplicative interactions between rs915894 and smoking, rs915894 and history of lung diseases, and rs915894 and family history of cancer, which all affect NSCLC survival. Conclusion This study demonstrated that rs915894 in NOTCH 4 may be a genetic marker for NSCLC prognosis in the Chinese population and that rs915894 may have an interactive relationship with epidemiologic factors.

Background Although cigarette smoking is a major risk factor for lung cancer, the incidence rate of lung cancer among non-smokers is notable. The etiology and potential mechanism of non-smoker lung cancer are worthy of further research. This study was designed to explore the collective effects of environmental factors and the relationship between environmental exposure index (EEI) and lung cancer among non-smokers by evaluating the joint effects among lung disease history, environmental factors, and family history of lung cancer without smoking confounders. Methods A total of 767 never-smoked lung cancer cases and 767 sex- and age-matched controls were selected from the department of Thoracic Surgery and Respiratory Medicine of three hospitals in Fujian, China. We used two methods to develop the EEI according to 12 statistically significant environmental risk factors. Restricted cubic spline (RCS) was applied to analyze the non-linear relationship between EEI and lung cancer in non-smokers. Combined effects, additive interaction, and multiplicative interaction were assessed among lung disease history, EEI, and family history of lung cancer to estimate susceptibility to develop lung cancer. Results Lung disease history, especially asthma, was significantly associated with an increased risk of lung cancer with an odds ratio (OR) for asthma history of 14.720 (95% CI: 1.877–115.449). Family history of lung cancer was related to susceptibility of lung cancer (OR = 3.347, 95% CI: 1.930–5.806). According to type of relatives and cancer, a parental or children’s history and a sibling’s history of lung cancer were significantly associated with an increased risk of lung cancer. The positive association between EEI and lung cancer was apparently stronger in those with lung disease history or family lung cancer history. Furthermore, there was a addictive interaction between EEI and lung disease history, and a possibly addictive interaction between EEI and family lung cancer history on development of lung cancer. Conclusions There were combined effects among lung disease history, environmental exposures, and family history of lung cancer toward susceptibility to lung cancer in Chinese non-smokers. Non-smokers who had a family history of lung cancer were at higher risk of lung cancer than non-smokers who had lung disease history. Non-smokers with family cancer history may obtain benefits from removal of environmental exposures and active treatment of lung disease.

Meta-analysis was performed on the Web of Science, PubMed, Embase, and Cochrane databases to evaluate the effect of epidermal growth factor receptor (EGFR) mutation status on programmed cell death protein 1/programmed death ligand 1 (PD-1/PD-L1) immune checkpoint inhibitors, and the association between EGFR mutation status and PD-L1 expression in non-small cell lung cancer (NSCLC) patients. Pooled effect (hazard ratio/odds ratio, HR/OR) with 95% confidence interval (CI) was calculated, and the source of heterogeneity was explored by subgroup analysis and meta-regression using Stata/SE 15.0. Meta-analysis of the association between EGFR mutation status and overall survival (OS) in NSCLC with immunotherapy was calculated from four randomized controlled trials. We found that immune checkpoint inhibitors significantly prolonged OS over docetaxel overall (HR 0.71, 95% CI 0.64–0.79) and in the EGFR wild type (HR = 0.67, 95% CI = 0.60–0.75), but not in the EGFR mutant subgroup (HR = 1.11, 95% CI = 0.80–1.52). Meta-analysis of the association between EGFR mutation status and PD-L1 expression in NSCLC included 32 studies. The pooled OR and 95% CI were 0.60 (0.46–0.80), calculated by random effects model. No source of heterogeneity was found in subgroup analysis. Sensitivity analysis was carried out with a fixed model, and the influence of a single study on the pooled results showed no significant change with robust meta-analysis methods. Harbord’s weighted linear regression test (P = 0.956) and Peters regression test (P = 0.489) indicated no significant publication bias. The limited benefit of single-agent PD-1/PD-L1 inhibitors in the second-line or later setting for EGFR-mutated NSCLC may be partly due to the lower expression of PD-L1.

Additional file of POU2F2 promotes the proliferation and motility of lung cancer cells by activating AGO1

Background: A systematic search was performed on the Web of Science, PubMed, Embase, and Cochrane databases. The meta-analysis was performed to evaluate the effect of epidermal growth factor receptor (EGFR) mutation status on programmed cell death protein 1/programmed death ligand 1 (PD-1/PD-L1) immune checkpoint inhibitors, and the association between EGFR mutation status and PD-L1 expression in non-small cell lung cancer (NSCLC) patients. Methods: Pooled effect (HR/OR) with 95% CI was calculated, the source of heterogeneity was explored by subgroup analysis and meta-regression using Stata/SE 15.0. Meta-analysis of the association between EGFR mutation status and overall survival in NSCLC with immunotherapy was calculated from four randomized controlled trials. Results: We found that immune checkpoint inhibitors significantly prolonged overall survival (OS) over docetaxel overall (HR: 0.71, 95% CI: 0.64-0.79) and in the EGFR wild-type (HR=0.67, 95% CI=0.60-0.75), but not in the EGFR-mutant subgroup (HR=1.11, 95% CI=0.80-1.52). Meta-analysis of the association between EGFR mutation status and PD-L1 expression in NSCLC included 32 studies. The pooled OR and 95% CI were 0.60 (0.46 0.80), calculated by random effects model. No source of heterogeneity was found in subgroup analysis. The sensitivity analysis was carried out with a fixed model, and the influence of a single study on the pooled results showed no significant change with robust meta-analysis methods. Harbord s weighted linear regression test (P=0.956) and Peters regression test (P=0.489) indicated no significant publication bias. Conclusions: The benefit of PD-1/PD-L1 immune checkpoint inhibitor treatment in patients with EGFR-mutated NSCLC is not obvious and may due to the lower expression of PD-L1. Funding: This study was supported by Fujian Program for Outstanding Young Researchers in University awarded by Education Department of Fujian (Grant Number 2017B019), Fujian Provincial Health Research Talents Training Programme Medical Innovation Project (Grant Number 2019- CX-33), Joint Funds for the innovation of science and Technology，Fujian province (Grant Number 2019Y9022), and Fujian Provincial Health Research Talents Training Programme Youth Research Project (Grant Number 2019-1- 58).The funding sponsors played no role in study design, data collection, data analysis, interpretation, writing of the report, and the decision to submit the paper for publication. Declaration of Interest: None to declare. Ethical Approval: This study was approved by the Institutional Review Board of Fujian Medical University (Fuzhou, China).

Background We investigated whether BCMO1 variants and dietary patterns are associated with lung cancer risk. Methods Case-control study including 1166 lung cancer cases and 1179 frequency matched controls was conducted for three BCMO1 variants (rs6564851, rs12934922, and rs7501331) and four dietary patterns were investigated. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (95% CIs). Results The rs6564851, rs12934922, and rs7501331 were not found to be associated with lung cancer risk (P > 0.05). In multivariable-adjusted models, compared to the lowest quartile of the score on the “fruits and vegetables” pattern, the highest quintile was associated with a 78.4% decreased risk (OR Q4 vs. Q1 = 0.216; 95% CI, 0.164–0.284; P for trend

Wei-Min Xiong,1 Qiu-Ping Xu,1 Ren-Dong Xiao,2 Zhi-Jian Hu,2 Lin Cai,1,3–5 Fei He1,3–51Department of Epidemiology and Health Statistics, School of Public Health, Fujian Medical University, Fuzhou 350108, People’s Republic of China; 2Department of Thoracic Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou 350001, People’s Republic of China; 3Fujian Provincial Key Laboratory of Tumor Microbiology, Fujian Medical University, Fuzhou 350108, People’s Republic of China; 4Key Laboratory of Ministry of Education for Gastrointestinal Cancer, Fujian Medical University, Fuzhou 350108, People’s Republic of China; 5Fujian Provincial Key Laboratory of Environment Factors and Cancer, Fujian Medical University, Fuzhou 350108, People’s Republic of ChinaAim: To explore the relationship between Chlamydia pneumonia (Cpn) infection and lung cancer using integrative methylome and transcriptome analyses.Methods: Twelve primary lung cancer patients who were positive for Cpn and twelve patients who were negative were selected for demographic, clinicopathological, and lifestyle matching. Genomic DNA and RNA were extracted and DNA methylation and mRNA levels were detected using the Infinium Human Methylation 450 Beadchip array and mRNA + lncRNA Human Gene Expression Microarray. We identified differentially expressed methylation and genes profiles.Results: Integrative analysis revealed an inverse correlation between differentially expressed genes and DNA methylation. Cpn-related lung cancer methylated genes (target genes) were introduced into the gene ontology and KEGG, PID, BioCarta, Reactome, BioCyc and PANTHER enrichment analyses using a q-value cutoff of 0.05 to identify potentially functional methylation of abnormal genes associated with Cpn infection. Gene sets enrichment analysis was evaluated according to MsigDB. Levels of differentially expressed methylated sites were quantitatively verified. The promoter methylation sites of 62 genes were inversely related to expression levels. According to the quantitative analysis of DNA methylation, the methylation level of the RIPK3 promoter region was significantly different between Cpn-positive cancerous and adjacent tissues, but not between Cpn-negative cancerous and adjacent tissues.Conclusion: Hypomethylation of the RIPK3 promoter region increases RIPK3 expression, leading to regulated programmed necrosis and activation of NF-κB transcription factors, which may contribute to the development and progression of Cpn-related lung cancer.Keywords: lung neoplasms, chlamydia pneumonia, DNA methylation, gene expression

Objective In this study, we analyzed the association between genetic variants of genes in the NOTCH signaling pathway and the prognosis of non-small-cell lung cancer (NSCLC) in the Chinese population. We also explored the interaction between genetic and epidemiological factors for the test group. Methods We performed genotyping of 987 NSCLC patients. Then, we used Cox proportional hazard models to analyze the associations between single-nucleotide polymorphisms (SNPs) and the prognosis of NSCLC. We employed Stata software to test the heterogeneity of associations between subgroups, and we analyzed the additive and multiplicative interactions between SNPs and epidemiologic factors. Results This work revealed the important prognostic and predictive value of rs915894 in the NOTCH4 gene, which may be regarded as a promising prognosis biomarker of NSCLC. Cox regression analysis indicated that the C allele of rs915894 is associated with longer survival and decreased risk of death in NSCLC (codominant model: adjusted HR =0.83, 95% CI =0.70–0.99; dominant model: adjusted HR =0.83, 95% CI =0.71–0.98). Additional stepwise regression analysis suggested that this SNP is an independently favorable factor for the prognosis of NSCLC (dominant model: adjusted HR =0.85, 95% CI =0.72–0.99). This protective effect is more pronounced for patients who are not smokers, have a history of other lung diseases, or have a family history of cancer. We also detected statistically significant additive and multiplicative interactions between rs915894 and smoking, rs915894 and history of lung diseases, and rs915894 and family history of cancer, which all affect NSCLC survival. Conclusion This study demonstrated that rs915894 in NOTCH4 may be a genetic marker for NSCLC prognosis in the Chinese population and that rs915894 may have an interactive relationship with epidemiologic factors.

// Wei-Min Xiong 1, 2, 3 , Qiu-Ping Xu 1, 2, 3 , Xu Li 4 , Ren-Dong Xiao 4 , Lin Cai 1, 2, 3 and Fei He 1, 2, 3 1 Department of Epidemiology and Health Statistics, School of Public Health, Fujian Medical University, Fuzhou, 350108, China 2 Fujian Provincial Key Laboratory of Tumor Microbiology, Fujian Medical University, Fuzhou, 350108, China 3 Key Laboratory of Ministry of Education for Gastrointestinal Cancer, Fujian Medical University, Fuzhou, 350108, China 4 Department of Thoracic Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, 350001, China Correspondence to: Fei He, email: ifeihe@163.com Lin Cai, email: cailin_prof@sina.com Keywords: lung neoplasms, human papillomavirus, meta-analysis, case-control study, cohort study Received: July 19, 2017 Accepted: September 21, 2017 Published: October 09, 2017 ABSTRACT To estimate the global attributable fraction of human papillomavirus (HPV) in lung cancer, we provided updated information through a system review and meta-analysis. We did a literature search on PubMed, Ovid and Web of Science to identify case-control studies and cohort studies that detected HPV in lung carcinomas. We included studies that tested 30 or more cases and were published before Feb 28, 2017. We collected information about gender, smoking status, HPV detection methods, HPV types, materials and clinical features. If it was not possible to abstract the required information directly from the papers, we contacted the authors. A meta-analysis was performed to calculate the pooled effect sizes ( OR/RR ) with 95% confidence intervals ( CI ) including subgroup analysis and meta-regression to explore sources of heterogeneity, by Stata 13.0 software. 36 case-control studies, contributing data for 6,980 cases of lung cancer and 7,474 controls from 17 countries and one cohort study with 24,162 exposed and 1,026,986 unexposed from China were included. HPV infection was associated with cancer of lung, pooled OR was 3.64 (95% CI : 2.60–5.08), calculated with the random-effects model. Pooled OR for allogeneic case-control studies, self-matched case-control studies and nested case-control studies were 6.71 (95% CI : 4.07–11.07), 2.59 (95% CI : 1.43–4.69) and 0.92 (95% CI : 0.63–1.36), respectively. Pooled OR for HPV 16 and HPV 18 infection, were 3.14 (95% CI : 2.07–4.76) and 2.25 (95% CI : 1.49–3.40), respectively. We also found that HPV infection may be associated with squamous cell carcinoma, adenocarcinoma and small cell carcinoma. There is evidence that HPV infection, especially HPV 16 and HPV 18 infection, significantly increase the risk of lung cancer. Future research needs to focus attention toward whether an HPV vaccine can effectively reduce the incidence of lung cancer.

The purpose of this study was to use the data on lung cancer in Han Chinese in Fujian province to explore the value of a generalized, linear model and to investigate the impact related to environment factors on lung cancer as well as the independent and interaction effects on the development of lung cancer. SAS 9.2 was used to build a generalized linear model to evaluate the influence factors and interaction of lung cancer on both smokers and non-smokers. Results showed that the relationship of the factors was multiplied. Under the logistic regression analysis, seven risk factors and nine risk factors were noticed in smokers or in non-smokers, respectively. Heavy smokers and lung diseases appeared a positive multiplying effect on smokers while passive smoking and fresh fruits showed positive multiplying effects on non-smokers. The generalized linear models could filter suitable models thus facilitating further research on the interaction between the two. It seemed easy to carry on the comprehensive and rational analysis on related epidemiological data.

This case–control study with a Fujian population investigated whether self-reported occupational and recreational physical activity may be associated with lung cancer. The population comprised 1622 patients with newly diagnosed primary lung cancer and 1622 age- and gender-matched healthy controls. High-intensity occupational physical activity was associated with significantly higher risk of lung cancer (OR = 1.354, 95% CI: 1.068–1.717), especially nonsmall cell lung carcinoma (OR = 1.384, 95% CI: 1.087–1.762). Moderate or low intensity recreational physical activity was associated with reduced risk of lung cancer. The protective effect of recreational physical activity was observed in current or former smokers, but not never-smokers, and in subjects with normal or high BMI, but not low BMI, as well as people without a history of chronic lung disease. The frequency of recreational physical activity was associated with a linear reduction in the risk of lung cancer (P