Risk of Lung Cancer and Past Use of Cannabis in Tunisia

Excision repair cross-complimentary group 2 (ERCC2) is one of the important DNA repair genes. ERCC2 codon 751 polymorphism has been shown to modulate cancer risk. We therefore assessed the relationship between the ERCC2 polymorphism and the susceptibility to lung cancer in nonsmoking females via a hospital-based case-control study. There were 105 lung cancer cases and matched healthy controls in this study. Information concerning demographic and risk factors was obtained, each person donated 2 ml blood for biomarker testing. ERCC2 genotypes were determined by PCR-RFLP method. All of the statistical analyses were performed with SPSS (v 12.0). All of the subjects in this study were nonsmoking females in Shenyang. There was significant difference between the frequencies of ERCC2 polymorphism in cancer cases and controls (P<0.05). The frequencies of ERCC2 751 Gln allele were 6.2% in controls and 13.8% in cancer cases. The individuals with Lys/Gln+Gln/Gln combined genotype were at an increased risk for lung cancer as compared with those carrying the Lys/Lys genotype (adjusted OR=2.80, 95%=CI 1.21−6.48). We analyzed the environmental risk factors for lung cancer in nonsmoking females. The cancer patients showed a higher prevalence of exposure to cooking fumes compared with controls (OR=2.44, P<0.05). Furthermore, an interaction between exposure to cooking fumes and the variant ERCC2 751 Gln allele on the risk of lung cancer was observed. Individuals with both risk genotype and exposure to cooking fumes had a higher risk of cancer than those with only one of them. The above findings indicate that the genetic polymorphism in the ERCC2 codon 751 is associated with the risk of lung cancer in nonsmoking females.

Studies on the relationships between inflammatory pathway genes and lung cancer risk have not included African-Americans and have only included a handful of genes. In a population-based case-control study on 198 African-American and 744 Caucasian women, we examined the association between 70 cytokine and cytokine receptor single-nucleotide polymorphisms (SNPs) and risk of non-small cell lung cancer (NSCLC). Unconditional logistic regression was used to estimate odds ratios and 95% confidence intervals in a dominant model adjusting for major risk factors for lung cancer. Separate analyses were conducted by race and by smoking history and history of chronic obstructive pulmonary disease among Caucasians. Random forest analysis was conducted by race. On logistic regression analysis, IL6 (interleukin 6), IL7R, IL15, TNF (tumor necrosis factor), and IL10 SNP were associated with risk of non-small cell lung cancer among African-Americans; IL7R and IL10 SNPs were also associated with risk of lung cancer among Caucasians. Although random forest analysis showed IL7R and IL10 SNPs as being associated with risk for lung cancer among African-Americans, it also identified TNFRSF10A SNP as an important predictor. On random forest analysis, an IL1A SNP was identified as an important predictor of lung cancer among Caucasian women. Inflammatory SNPs differentially predicted risk for NSCLC according to race, as well as based on smoking history and history of chronic obstructive pulmonary disease among Caucasian women. Pathway analysis results are presented. Inflammatory pathway genotypes may serve to define a high risk group; further exploration of these genes in minority populations is warranted.

Lung cancer is one of malignant tumors to hurt human health. It has been known that the development of lung cancer may be associated with genetic polymorphism of some lung cancer related genes. The aim of this study is to explore the susceptibility to lung cancer in relation to CYP1A1 and GSTM1 genetic polymorphisms in population of Inner Mongolia. CYP1A1 and GSTM1 genetic polymorphisms were determined by PCR-RFLP in 163 lung cancer cases and healthy controls respectively. The frequencies of CYP1A1 variation genotype (vt/vt) and GSTM1(-) were 36.8% and 65.0% in lung cancer cases and 19.0% and 48.9% in healthy controls respectively. Statistical tests showed significant difference in the frequencies between the two groups (Chi-Square =12.82, P=0.0001; Chi-Square = 9.78, P=0.002). The risk of lung cancer with CYP1A1 variation genotype was significantly higher than those of controls (OR= 2.48, 95% CI=1.51-4.08). The individuals who carried with GSTM1-null genotype had a high risk of lung cancer (OR=2.03, 95% CI=1.30-3.17). Combined analysis of the polymorphisms showed that percentage of CYP1A1(vt/vt)/GSTM1(-) in lung cancer and control groups was 28.8% and 8.0% respectively (Chi-Square = 23.883, P=0.0001). The people who carried with CYP1A1(vt/vt)/GSTM1(-) had a high risk of lung cancer (OR=4.90, 95% CI=2.50-9.83). Pearson Chi-Square of sex differential showed there was no significance between the homozygous variation genotype of CYP1A1/GSTM1(-) and the other genotypes of CYP1A1/GSTM1(-) neither in lung cancer group (Chi-Square=0.797, P=0.372) nor in control group (Chi-Square=0.670, P=0.761). Statistical tests showed that susceptibility to lung cancer was related to smoking (Chi-Square = 14.197, P=0.000), the risk of lung cancer in smoking individuals raised remarkably (OR=2.33, 95% CI=1.50-3.62). There may be a synergetic interaction between CYP1A1 variation genotype (vt/vt) and smoking on the elevated susceptibility to lung cancer (Chi-Square = 23.843, P=0.000), the smokers who carried with CYP1A1 (vt/vt) had a significantly higher risk of lung cancer (OR=4.44, 95% CI=2.40-8.32, Chi-Square = 23.843, P= 0.000). So did the GSTM1(-) and smoking on the elevated susceptibility to lung cancer, the significantly higher risk of lung cancer had also been found in those smokers who carried with GSTM1(-) (OR=7.32, 95% CI=3.39-15.50, Chi-Square = 36.708,P=0.000). The polymorphisms of CYP1A1 vt/vt and GSTM1(-) are the risk factors in lung cancer of Inner Mongolia. Smoking is also related to the susceptibility to lung cancer. There may be a synergetic interaction between CYP1A1 (vt/vt) and GSTM1(-) on the elevated susceptibility of lung cancer. So do the CYP1A1 (vt/vt), GSTM1(-) and smoking.

Leisure Time Activities and Lung Cancer

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. 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. 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). 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.

Although large-scale studies, including meta-analyses, on the association between alcohol consumption and lung cancer have been reported, the risk of lung cancer in extremely high consumption groups (>or=450 g ethanol/week) in both current smokers and nonsmokers remains unclear. Here, we investigated the association between alcohol consumption and lung cancer incidence. We conducted a population-based prospective cohort study in 46,347 Japanese men aged 40-69 years with no history of cancer at baseline in 1990-1994. We used Cox proportional hazards regression analysis to estimate the hazard ratio (HR) and 95% confidence interval (CI) of lung cancer incidence according to alcohol consumption. During the 14-year follow-up period, we documented 651 cases of lung cancer. We found a positive association between alcohol consumption and lung cancer risk confined to current smokers. Compared with occasional drinkers, the multivariate HRs (95% CI) in the highest category (>or=450 g ethanol/week) were 1.31 (0.89-1.94) among total participants, 0.58 (0.26-1.30) (p for trend = 0.49) among nonsmokers, and 1.69 (1.05-2.72) (p for trend = 0.02) among current smokers. Among this population with a large variation in alcohol consumption, alcohol consumption was not an independent risk factor for lung cancer except for current smokers.

BackgroundLung cancer is a common malignancy in rheumatoid arthritis (RA)1,2. Since smoking is a risk factor for both (seropositive) RA and lung cancer, it remains unclear whether RA, in itself,...

Previous studies have shown that asthma is a risk factor for lung cancer, while the mechanisms involved remain unclear. We attempted to further explore the association between asthma and non-small cell lung cancer (NSCLC) via bioinformatics analysis. We obtained GSE143303 and GSE18842 from the GEO database. Lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) groups were downloaded from the TCGA database. Based on the results of differentially expressed genes (DEGs) between asthma and NSCLC, we determined common DEGs by constructing a Venn diagram. Enrichment analysis was used to explore the common pathways of asthma and NSCLC. A protein-protein interaction (PPI) network was constructed to screen hub genes. KM survival analysis was performed to screen prognostic genes in the LUAD and LUSC groups. A Cox model was constructed based on hub genes and validated internally and externally. Tumor Immune Estimation Resource (TIMER) was used to evaluate the association of prognostic gene models with the tumor microenvironment (TME) and immune cell infiltration. Nomogram model was constructed by combining prognostic genes and clinical features. 114 common DEGs were obtained based on asthma and NSCLC data, and enrichment analysis showed that significant enrichment pathways mainly focused on inflammatory pathways. Screening of 5 hub genes as a key prognostic gene model for asthma progression to LUAD, and internal and external validation led to consistent conclusions. In addition, the risk score of the 5 hub genes could be used as a tool to assess the TME and immune cell infiltration. The nomogram model constructed by combining the 5 hub genes with clinical features was accurate for LUAD. Five-hub genes enrich our understanding of the potential mechanisms by which asthma contributes to the increased risk of lung cancer.

BACKGROUND: Cigarette smoking is closely related to both lung cancer and chronic obstructive pulmonary disease. The incidence of lung cancer is higher in patients with obstructive ventilatory impairment than in patients without obstructive ventilatory impairment regardless of smoking. So, obstructive ventilatory impairment is suspected as an independent risk factor of lung cancer. METHODS: For the evaluation of the role of obstructive ventilatory impairment as a risk factor of lung cancer, a total of 73 cases comprising 47 cases of malignant and 26 benign solitary pulmonary nodule were analyzed retrospectively. A comparative study of analysis of forced expiratory volume curves and frequencies of obstructive ventilatory impairment were made between cases with malignant and benign nodules. RESULTS: In comparison of vital capacity and parameters derived from forced expiratory volume curve between two groups, VC, FVC and FEV1 were not significantly different whereas FEV1/FVC% and FEF 25-75 % showed a significant decrease in the cases with malignant nodule. The frequency of obstructive ventilatory impairment determined by pulmonary function test was significantly higher in the cases with malignant nodule (23.4%) than in benign nodule(3.8%). When the risk for lung cancer was examined by the presence or absence of obstructive ventilatory impairment using the logistic regression analysis, the unadjusted relative risk for the lung cancer of obstructive ventilatory impairment was 17.17. When the effect of smoking and age were considered, the relative risk was to 8.13. CONCLUISON: These findings suggest that an obstructive ventilatory impairment is a risk factor of lung cancer.

Amid shifting tobacco policies and escalating air pollution levels, Lung Cancer (LC) risk factors have changed notably. Continuous assessment of these risk factors is necessary. This study compares trends in tobacco, air pollution, and asbestos-associated Age-Standardized Mortality Rates (ASMR) from Trachea, Bronchus, and Lung (TBL) Cancer across the top ten most populated countries (2023 censuses) and globally. We extracted overall and risk-factor-associated TBL cancer ASMR of the ten most populated countries for 1990-2019 from the Global Burden of Disease (GBD) database using the dedicated results tool (http://ghdx.healthdata.org/gbd-results-tool). GBD mapped the mortality data related to ICD codes (C33-C34, D02.1-D02.2, D38.1, 162-162.9, 231.1, 231.2, 231.8, 235.7 from ICD10 and B101 from ICD9). Tobacco, occupational exposure to asbestos and air pollution (ambient particulate matter and household air pollution) associated TBL cancer mortality data were extracted to evaluate the trends based on risk factors. We calculated relative changes in ASMRs between 1990 and 2019 for each sex in each country for each risk factor. Joinpoint regression analysis was performed to calculate the Estimated Annual Percentage Change (EAPC) and its corresponding 95% confidence interval (CI) for each line segment, allowing for trend assessment. Globally, TBL Cancer mortality has decreased by 8%, with a decrease for males but an increase for females. Globally, both tobacco and air pollution-associated TBL cancer ASMR have decreased. While tobacco-associated ASMR has increased in China and Indonesia, air pollution-associated ASMR has also increased in China, India, Pakistan, and Nigeria. On stratification, while PM-associated mortality increased by 25% globally, household-associated TBL cancer ASMR decreased by 62%. China had the highest PM-associated TBL Cancer in 2019 (8.8/100,000), twice higher than the global average. Despite a decline in asbestos-associated TBL cancer ASMR from 8.91/100,000 to 6.0/100,000, the rate in the United States remained twice higher than the global average for the entire study period. Tobacco-associated TBL cancer mortality is declining but still predominant. Ambient particulate matter-associated TBL cancer mortality is rising, requiring policy and awareness efforts. Expanding access to preventive services and addressing underlying risk factors are essential steps required toward reducing lung cancer mortality at the global level. This study did not receive any funding support.

BackgroundObservational studies indicate that periodontal disease may increase the risk of colorectal, lung, and pancreatic cancers. Using a 2-sample Mendelian randomization (MR) analysis, we assessed whether a genetic predisposition index for periodontal disease was associated with colorectal, lung, or pancreatic cancer risks.MethodsOur primary instrument included single nucleotide polymorphisms with strong genome-wide association study evidence for associations with chronic, aggressive, and/or severe periodontal disease (rs729876, rs1537415, rs2738058, rs12461706, rs16870060, rs2521634, rs3826782, and rs7762544). We used summary-level genetic data for colorectal cancer (n = 58 131 cases; Genetics and Epidemiology of Colorectal Cancer Consortium, Colon Cancer Family Registry, and Colorectal Transdisciplinary Study), lung cancer (n = 18 082 cases; International Lung Cancer Consortium), and pancreatic cancer (n = 9254 cases; Pancreatic Cancer Consortia). Four MR approaches were employed for this analysis: random-effects inverse‐variance weighted (primary analyses), Mendelian Randomization-Pleiotropy RESidual Sum and Outlier, simple median, and weighted median. We conducted secondary analyses to determine if associations varied by cancer subtype (colorectal cancer location, lung cancer histology), sex (colorectal and pancreatic cancers), or smoking history (lung and pancreatic cancer). All statistical tests were 2-sided.ResultsThe genetic predisposition index for chronic or aggressive periodontitis was statistically significantly associated with a 3% increased risk of colorectal cancer (per unit increase in genetic index of periodontal disease; P = .03), 3% increased risk of colon cancer (P = .02), 4% increased risk of proximal colon cancer (P = .01), and 3% increased risk of colorectal cancer among females (P = .04); however, it was not statistically significantly associated with the risk of lung cancer or pancreatic cancer, overall or within most subgroups.ConclusionsGenetic predisposition to periodontitis may be associated with colorectal cancer risk. Further research should determine whether increased periodontitis prevention and increased cancer surveillance of patients with periodontitis is warranted.

BackgroundThe effects of vegetable preference and leisure-time physical activity (LPA) on cancer have been inconsistent. We examined the effects of dietary preference and physical activity, as well as their combined effect on cancer risk.MethodsThis prospective cohort study included 444,963 men, older than 40 years, who participated in a national health examination program begun in 1996. Based on the answer to the question "What kind of dietary preference do you have?" we categorized dietary preference as (1) vegetables, (2) mixture of vegetables and meat, and (3) meats. We categorized LPA as low (< 4 times/wk, < 30 min/session), moderate (2–4 times/wk, ≥ 30 min/session or ≥ 5 times/wk, < 30 min/session), or high (≥ 5 times/wk, ≥ 30 min/session). We obtained cancer incidence data for 1996 through 2002 from the Korean Central Cancer Registry. We used a standard Poisson regression model with a log link function and person-time offset to estimate incidence and relative risk..ResultsDuring the 6-year follow-up period, we identified 14,109 cancer cases. Multivariate analysis revealed that a preference for vegetables or a mixture of vegetables and meat as opposed to a preference for meat played a significant protective role against lung cancer incidence (aRR, 0.81; 95% confidence interval [CI], 0.68–0.98). Compared with the low LPA group, subjects with moderate-high LPA had a significantly lower risk for stomach (aRR, 0.91; 95%CI, 0.86–0.98), lung (aRR, 0.83; 95%CI, 0.75–0.92), and liver (aRR, 0.88; 95%CI, 0.81–0.95) cancer. Among current smokers, the combined moderate-high LPA and vegetable or mixture of vegetables and meat preference group showed a 40% reduced risk of lung cancer (aRR, 0.60; 95%CI, 0.47–0.76) compared with the combined low LPA and meat preference group. Among never/former smokers, subjects with moderate-high LPA and a preference for vegetables or a mixture of vegetables and meat showed reduced stomach cancer risk (aRR, 0.72; 95%CI, 0.54–0.95).ConclusionOur findings add to the evidence of the beneficial effects of vegetable preference on lung cancer risk and of physical activity on lung, stomach, and liver cancer risk. Additionally, vegetable preference combined with LPA might significantly reduce lung and stomach cancer risk.

In this work the lifetime relative risks (LRR) of lung cancer due to exposure to indoor 222Rn on the Mexican population is calculated. Cigarette smoking is the number one risk factor for lung cancer (LC), because that, to calculate the number of cases of LC due to exposure to 222Rn is necessary considers the number of cases of LC for smoking cigarette. The lung cancer mortality rates published by the "Secretaría de Salud" (SSA), the mexican population data published by the "Consejo Nacional de Población" (CONAPO), smoking data in the mexican population, published by the "Comisión Nacional Contra las Adicciones" (CONADIC), the "Organización Panamericana de la Salud" (OPS) and indoor 222Rn concentrations in Mexico published in several recent studies are used. To calculate the lifetime relative risks (LRR) for different segments of the Mexican population, firstly the Excess Relative Risk (ERR) is calculated using the method developed by the BEIR VI committee and subsequently modified by the USEPA and published in the report "EPA Assessment of Risks from Radon in Homes". The excess relative risks were then used to calculate the corresponding lifetime relative risks, again using the method developed by the BEIR VI committee. The lifetime relative risks for Mexican male and female eversmokers and Mexican male and female never-smokers were calculated for radon concentrations spanning the range found in recent studies of indoor radon concentrations in Mexico. The lifetime relative risks of lung cancer induced by lifetime exposure to the mexican average indoor radon concentration were estimated to be 1.44 and 1.40 for never-smokers mexican females and males respectively, and 1.19 and 1.17 for ever-smokers Mexican females and males respectively. The Mexican population LRR values obtained in relation to the USA and Canada LRR published values in ever-smokers for both gender are similar with differences less than 4%, in case of never-smokers in relation with Canada population the differences in LRR values are less than 2% and in never-smokers for the USA population the differences in LRR values compared with the Mexican population are about 10%.

Two adult cases of the Fanconi syndrome are described, in each of which there was abnormal urinary excretion of immunoglobulin kappa-chain. The significance of this finding is discussed in relation to the recognized association between multiple myeloma and the Fanconi syndrome.

Risk factors of lung cancer unrelated to smoking are not well-studied, especially among women. Family history has been shown to play a role in predisposing individuals to lung cancer, but this relationship has not been investigated in the Southeast Asian population. A total of 1159 women were recruited in a case–control study conducted in public hospitals in Singapore from 2005 to 2008. After excluding participants with incomplete family history information, 374 cases and 785 controls remained in the final analysis. Adjusted odds ratios (aORs) and 95% confidence intervals (CIs) were calculated using logistic regression, adjusting for potential confounders. Overall, family history of lung cancer was associated with a higher risk for lung cancer (aOR 2.08, 95% CI 1.25–3.47). When stratified by smoking status, a significant association was observed among never-smokers (aOR 2.78, 95% CI 1.57–4.90). Further stratification by fruit consumption identified a significant association between family history of lung cancer and higher risk of lung cancer among never-smokers who had low fruit consumption (aOR 3.09, 95% CI 1.37–7.01). Our findings suggest that family history of lung cancer is a significant risk factor for lung cancer in Singaporean Chinese women, especially among never-smokers.