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  • LUNG-CANCER  (7)
  • 1
    Keywords: CANCER ; LUNG ; EMPHYSEMA ; FOLLOW-UP ; lung cancer ; LUNG-CANCER ; NETWORKS ; DEATH ; DISEASE ; DNA adducts ; EXPOSURE ; RISK ; GENES ; TIME ; DNA ; AIR-POLLUTION ; ASSOCIATION ; POLYMORPHISMS ; AGE ; REPAIR ; smoking ; leukemia ; bladder cancer ; BLADDER-CANCER ; cancer risk ; DAMAGE ; POLYCYCLIC AROMATIC-HYDROCARBONS ; DNA-DAMAGE ; RECRUITMENT ; ADDUCTS ; case-control studies ; EPIC ; nutrition ; QUESTIONNAIRE ; WHITE BLOOD-CELLS ; DNA-ADDUCTS ; case-control study ; DETERMINANTS ; monitoring ; GSTM1 ; LEVEL ; ADDUCT ; case control studies ; INTERVAL ; DNA damage ; DNA ADDUCT ; ABILITY ; GENDER ; OUTDOOR AIR-POLLUTION ; OZONE
    Abstract: Objectives were to investigate prospectively the ability of DNA adducts to predict cancer and to study the determinants of adducts, especially air pollutants. DNA adducts were measured in a case-control study nested in the European Prospective Investigation into Cancer and Nutrition (EPIC investigation. Cases included newly diagnosed lung cancer (n = 115), upper respiratory cancers (pharynx and larynx, n 82), bladder cancer (n = 124), leukemia (n = 166), and chronic obstructive pulmonary disease or emphysema deaths (n = 77) accrued after a median follow-up of 7 years among the EPIC former smokers and never-smokers. Three controls per case were matched for questionnaire analyses and two controls per case for laboratory analyses. Matching criteria were gender, age, smoking status, country of recruitment, and follow-up time. Individual exposure to air pollution was assessed using concentration data from monitoring stations in routine air quality monitoring networks. Leukocyte DNA adducts were analyzed blindly using (32)p postlabeling technique. Adducts were associated with the subsequent risk of lung cancer, with an odds ratio (OR) of 1.86 [95% confidence interval (95% CI), 0.88-3.931 when comparing detectable versus nondetectable adducts. The association with lung cancer was stronger in never-smokers (OR, 4.04; 95% CI, 1.06-15.42) and among the younger age groups. After exclusion of the cancers occurring in the first 36 months of follow-up, the OR was 4.16 (95% CI, 1.24-13.88). A positive association was found between DNA adducts and ozone (O-3) concentration. Our prospective study suggests that leukocyte DNA adducts may predict lung cancer risk of never-smokers. Besides, the association of DNA adduct levels with O-3 indicates a possible role for photochemical smog in determining DNA damage
    Type of Publication: Journal article published
    PubMed ID: 16140979
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  • 2
    Keywords: CANCER ; LUNG ; PATHWAY ; PATHWAYS ; PHASE-I ; lung cancer ; LUNG-CANCER ; COHORT ; RISK ; ENZYMES ; GENE ; GENES ; PATIENT ; RISK-FACTORS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; SUSCEPTIBILITY ; VARIANTS ; BREAST-CANCER ; DELETION ; NO ; STRESS ; AGE ; SNP ; smoking ; leukemia ; ACUTE LYMPHOBLASTIC-LEUKEMIA ; bladder cancer ; BLADDER-CANCER ; cancer risk ; gene-environment interaction ; INVOLVEMENT ; case-control studies ; TOBACCO ; OXIDATIVE STRESS ; European Prospective Investigation into Cancer and Nutrition ; nutrition ; glutathione-S-transferase ; DNA-ADDUCTS ; SINGLE ; ONCOLOGY ; case control study ; case-control study ; ASSOCIATIONS ; PATTERN ; VARIANT ; ALLELE ; SINGLE NUCLEOTIDE POLYMORPHISMS ; SNPs ; interaction ; GSTM1 ; METHYLENETETRAHYDROFOLATE REDUCTASE ; MTHFR ; ALLELES ; case control studies ; ENVIRONMENTAL TOBACCO-SMOKE ; INTERVAL ; ENZYME ; methods ; PHASE ; single-nucleotide ; pooled analysis ; prospective ; CANDIDATE ; NEVER SMOKERS ; CANCERS ; CANCER-RISK ; Phase I ; SET ; case control ; METABOLIC PATHWAYS ; GENETIC-SUSCEPTIBILITY ; nonsmokers ; METHYLENE-TETRAHYDROFOLATE REDUCTASE ; metabolic genes ; NULL-GENOTYPE
    Abstract: Background: We chose a set of candidate single nucleotide polymorphisms (SNPs) to investigate gene-environment interactions in three types of cancer that have been related to air pollution (lung, bladder and myeloid leukemia). Patients and methods: The study has been conducted as a nested case-control study within the European Prospective Investigation into Cancer and Nutrition cohort (409 cancer cases and 757 matched controls). We included never and ex-smokers. SNPs were in genes involved in oxidative stress, phase I metabolizing genes, phase 11 metabolizing genes and methylenetetrahydrofolate reductase (MTHFR). Results: The most notable findings are: GSTM1 deletion and bladder cancer risk [odds ratio (OR) = 1.60; 95% confidence interval 1.00-2.56]; CYP1A1 and leukemia (2.22, 1.33-3.70; heterozygotes); CYP1B1 and leukemia (0.47, 0.27-0.84; homozygotes); MnSOD and leukemia (1.91, 1.08-3.38; homozygotes) and NQO1 and lung cancer (8.03, 1.73-37.3; homozygotes). Other statistically significant associations were found in subgroups defined by smoking habits (never or ex-smokers), environmental tobacco smoke or gender, with no obvious pattern. When gene variants were organized according to the three main pathways, the emerging picture was of a strong involvement of combined phase I enzymes in leukemia, with an OR of 5 (1.63-15.4) for those having three or more variant alleles. The association was considerably stronger for leukemias arising before the age of 55
    Type of Publication: Journal article published
    PubMed ID: 17496311
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  • 3
    Keywords: CANCER ; LUNG-CANCER ; COHORT ; DNA adducts ; EXPOSURE ; RISK ; DNA ; BIOMARKERS ; colon ; RATS ; CONTRAST ; BINDING ; ASSOCIATION ; COLORECTAL-CANCER ; BLADDER-CANCER ; cancer risk ; POLYCYCLIC AROMATIC-HYDROCARBONS ; COLON-CANCER ; MULTIVARIATE ; ADDUCTS ; CARCINOGENS ; DIET ; DIETARY ; ALCOHOL ; EPIC ; nutrition ; SMOKERS ; FOOD ; GUIDELINES ; VITAMIN-E ; DNA-ADDUCTS ; REGRESSION ; air pollution ; prospective studies ; N-NITROSAMINES ; LEVEL ; biomarker ; analysis ; prospective ; prospective study ; correlation ; BMI ; CANCER-RISK ; ENGLAND ; non-smokers ; AMINE ; gastrointestinal ; European Prospective Investigation into Cancer ; fibre intake ; haemoglobin adducts ; RESISTANT STARCH
    Abstract: In contrast to some extensively examined food mutagens, for example, aflatoxins, N-nitrosamines and heterocyclic amines, some other food contaminants, in particular polycyclic aromatic hydrocarbons (PAH) and other aromatic compounds, have received less attention. Therefore, exploring the relationships between dietary habits and the levels of biomarkers related to exposure to aromatic compounds is highly relevant. We have investigated in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort the association between dietary items (food groups and nutrients) and aromatic DNA adducts and 4-aminobiphenyl-Hb adducts. Both types of adducts are biomarkers of carcinogen exposure and possibly of cancer risk, and were measured, respectively, in leucocytes and erythrocytes of 1086 (DNA adducts) and 190 (Hb adducts) non-smokers. An inverse. statistically significant, association has been found between DNA adduct levels and dietary fibre intake (P=0.02), vitamin E (P =0.04) and alcohol (P=0.03) but not with other nutrients or food groups. Also, an inverse association between fibre and fruit intake, and BMI and 4-aminobiphenyl-Hb adducts (P=0.03, 0.04, and 0.03 respectively) was observed. After multivariate regression analysis these inverse correlations remained statistically significant, except for the correlation adducts v. fruit intake. The present study suggests that fibre intake in the usual range can modify the level of DNA or Hb aromatic adducts, but Such role seems to be quantitatively modest. Fibres could reduce the formation of DNA adducts in different manners, by diluting potential food mutagens and carcinogens in the gastrointestinal tract, by speeding their transit through the colon and by binding carcinogenic substances
    Type of Publication: Journal article published
    PubMed ID: 18275627
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  • 4
    Keywords: CANCER ; LUNG ; MODEL ; PATHWAY ; PATHWAYS ; lung cancer ; LUNG-CANCER ; COHORT ; cohort studies ; cohort study ; DEATH ; DISEASE ; DISEASES ; DNA adducts ; RISK ; RISKS ; GENE ; GENES ; DNA ; RISK-FACTORS ; AIR-POLLUTION ; polymorphism ; POLYMORPHISMS ; BREAST-CANCER ; LESIONS ; DESIGN ; DNA-REPAIR ; REPAIR ; risk factors ; smoking ; bladder cancer ; BLADDER-CANCER ; cancer risk ; MUTATIONS ; ADDUCTS ; case-control studies ; OXYGEN ; DNA repair ; EXCISION-REPAIR ; reactive oxygen species ; case-control study ; VARIANT ; air pollution ; INCREASE ; SINGLE NUCLEOTIDE POLYMORPHISMS ; FUNCTIONAL-CHARACTERIZATION ; XPD POLYMORPHISMS ; case control studies ; INTERVAL ; RISK-FACTOR ; CANCER-RISK ; N-NITROSO COMPOUNDS ; BASAL-CELL CARCINOMA ; CHROMOSOME 19Q13.2-3 ; GENE XRCC3
    Abstract: Environmental carcinogens contained in air pollution, such as polycyclic aromatic hydrocarbons, aromatic amines or N-nitroso compounds, predominantly form DNA adducts but can also generate interstrand cross-links and reactive oxygen species. If unrepaired, such lesions increase the risk of somatic mutations and cancer. Our study investigated the relationships between 22 polymorphisms (and their haplotypes) in 16 DNA repair genes belonging to different repair pathways in 1094 controls and 567 cancer cases (bladder cancer, 131; lung cancer, 134; oral-pharyngeal cancer, 41; laryngeal cancer, 47; leukaemia, 179; death from emphysema and chronic obstructive pulmonary disease, 84). The design was a case-control study nested within a prospective investigation. Among the many comparisons, few polymorphisms were associated with the diseases at the univariate analysis: XRCC1-399 Gln/Gln variant homozygotes [odds ratios (OR) = 2.20, 95% confidence intervals (CI) = 1.16-4.17] and XRCC3-241 Met/Met homozygotes (OR = 0.51, 95% CI = 0.27-0.96) and leukaemia. The recessive model in the stepwise multivariate analysis revealed a possible protective effect of XRCC1-399Gln/Gln in lung cancer (OR = 0.22, 95% CI = 0.05-0.98), and confirmed an opposite effect (OR = 2.47, 95% CI = 1.02-6.02) in the leukaemia group. Our results also suggest that the XPD/ERCC1-GAT haplotype may modulate leukaemia (OR = 1.28, 95% CI = 1.02-1.61), bladder cancer (OR = 1.38, 95% CI = 1.06-1.79) and possibly other cancer risks. Further investigations of the combined effects of polymorphisms within these DNA repair genes, smoking and other risk factors may help to clarify the influence of genetic variation in the carcinogenic process
    Type of Publication: Journal article published
    PubMed ID: 16308313
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  • 5
    Keywords: CANCER ; BLOOD ; LUNG ; EMPHYSEMA ; LUNG-CANCER ; DEATH ; DISEASE ; DISEASES ; EXPOSURE ; HEPATOCELLULAR-CARCINOMA ; POPULATION ; RISK ; BIOMARKERS ; ASSOCIATION ; FREQUENCY ; WOMEN ; CIGARETTE-SMOKING ; leukemia ; BLADDER-CANCER ; ADDUCTS ; TOBACCO ; INDIVIDUALS ; PERIPHERAL-BLOOD ; nutrition ; DNA-ADDUCTS ; TOBACCO-SMOKE ; CHEMICAL CARCINOGENS ; protein adducts ; LEVEL ; ADDUCT ; AFLATOXIN EXPOSURE ; biomarker ; case control studies ; ENVIRONMENTAL TOBACCO-SMOKE ; HEMOGLOBIN ADDUCTS ; INTERVAL
    Abstract: The aim of this study was to evaluate whether biomarkers of environmental tobacco smoke exposure [i.e, 4-aminobiphenyl-hemoglobin (4-ABP-Hb) adducts] were predictive of the risk of tobacco-related cancers and diseases. We did a case control study nested within the European Prospective Investigation into Cancer and Nutrition, involving 190 controls and 149 cases (incident cancer of the lung, bladder, pharynx, larynx, oral cavity, leukemias, and chronic obstructive pulmonary disease or emphysema deaths). All individuals were never smokers or ex smokers for 〉 10 years. 4-ABP-Hb adducts were analyzed in peripheral blood collected before the onset of the disease (median, 7 years). Overall, 4-ABP-Hb adducts were higher, although not statistically significantly so, in cases (as a whole) than controls. In the control population, high fruit and vegetable consumption significantly lowered the frequency of detectable adducts (Fisher's exact test, P = 0.025). Restricting the analysis to women, 4-ABP-Hb adducts were higher in cases than controls (Mann-Whitney P = 0.036) and the odds ratio (OR) for the presence/absence of adducts was 2.42 [95% confidence interval (95% CI), 1.18-4.981. Moreover, the association of adducts with the individual cancer types was stronger in women than in the whole study population, although statistically significant only for leukemias (OR, 2.77; 95% CI, 1.06-7.20). The results provide some evidence that women may be more susceptible to environmental tobacco smoke, as suggested by their higher adduct levels. The most important finding of this prospective study is that, at least in women, 4-ABP-Hb adducts may help identify subjects at high risk of cancers related to environmental tobacco smoke exposure
    Type of Publication: Journal article published
    PubMed ID: 16172219
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  • 6
    Keywords: CANCER ; LUNG ; DIAGNOSIS ; FOLLOW-UP ; lung cancer ; LUNG-CANCER ; COHORT ; EXPOSURE ; MORTALITY ; RISK ; TIME ; AIR-POLLUTION ; ASSOCIATION ; AGE ; smoking ; COUNTRIES ; RECRUITMENT ; ADDUCTS ; case-control studies ; EPIC ; nutrition ; SMOKERS ; case-control study ; air pollution ; case control studies ; INTERVAL ; GENDER ; occupational exposures ; prospective study ; EXPOSURES ; SO2 ; AMBIENT ; POLLUTANTS
    Abstract: To estimate the relationship between air pollution and lung cancer, a nested case-control study was set up within EPIC (European Prospective Investigation on Cancer and Nutrition). Cases had newly diagnosed lung cancer, accrued after a median follow-up of 7 years among the EPIC exsmokers (since at least 10 years) and never smokers. Three controls per case were matched. Matching criteria were gender, age (+/- 5 years), smoking status, country of recruitment and time elapsed between recruitment and diagnosis. We studied residence in proximity of heavy traffic roads as an indicator of exposure to air pollution. In addition, exposure to air pollutants (NO2, PM10, SO2) was assessed using concentration data from monitoring stations in routine air quality monitoring networks. Cotinine was measured in plasma. We found a nonsignificant association between lung cancer and residence nearby heavy traffic roads (odds ratio = 1.46, 95% confidence interval, CI, 0.89-2.40). Exposure data for single pollutants were available for 197 cases and 556 matched controls. For NO2 we found an odds ratio of 1.14 (95% CI, 0.78-1.67) for each increment of 10 mu g/m(3), and an odds ratio of 1.30 (1.02-1.66) for concentrations greater than 30 mu g/m(3). The association with NO2 did not change after adjustment by cotinine and additional potential confounders, including occupational exposures. No clear association was found with other pollutants. (c) 2006 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16463382
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  • 7
    Keywords: CANCER ; human ; LUNG ; MODEL ; lung cancer ; LUNG-CANCER ; COHORT ; cohort study ; DISEASE ; DISEASES ; EXPOSURE ; GENE ; GENES ; COMPLEX ; COMPLEXES ; DNA ; REDUCTION ; ASSOCIATION ; FREQUENCY ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; VARIANTS ; FREQUENCIES ; NUMBER ; REPAIR ; leukemia ; ACUTE LYMPHOBLASTIC-LEUKEMIA ; BLADDER-CANCER ; REGION ; DNA repair ; DNA-REPAIR GENES ; VARIANT ; FUNCTIONAL-CHARACTERIZATION ; CATECHOL-O-METHYLTRANSFERASE ; METHYLENETETRAHYDROFOLATE REDUCTASE ; prospective ; LUNG-CANCER RISK ; VARIABLES ; metabolic gene polymorphisms ; METABOLISM GENES
    Abstract: It is becoming increasingly evident that single-locus effects cannot explain complex multifactorial human diseases like cancer. We applied the multi-factor dimensionality reduction (MDR) method to a large cohort study on gene-environment and gene-gene interactions. The study (case-control nested in the EPIC cohort) was established to investigate molecular changes and genetic susceptibility in relation to air pollution and environmental tobacco smoke (ETS) in non-smokers. We have analyzed 757 controls and 409 cases with bladder cancer (n = 124), lung cancer (n = 116) and myeloid leukemia (n = 169). Thirty-six gene variants (DNA repair and metabolic genes) and three environmental exposure variables (measures of air pollution and ETS at home and at work) were analyzed. Interactions were assessed by prediction error percentage and cross-validation consistency (CVC) frequency. For lung cancer, the best model was given by a significant gene-environment association between the base excision repair (BER) XRCC1-Arg399Gln polymorphism, the double-strand break repair (DSBR) BRCA2-Asn372His polymorphism and the exposure variable 'distance from heavy traffic road', an indirect and robust indicator of air pollution (mean prediction error of 26%, P 〈 0.001, mean CVC of 6.60, P = 0.02). For bladder cancer, we found a significant 4-loci association between the BER APE1-Asp148Glu polymorphism, the DSBR RAD52-3'-untranslated region (3'-UTR) polymorphism and the metabolic gene polymorphisms COMT-Val158Met and MTHFR-677C 〉 T (mean prediction error of 22%, P 〈 0.001, mean CVC consistency of 7.40, P 〈 0.037). For leukemia, a 3-loci model including RAD52-2259C 〉 T, MnSOD-Ala9Val and CYP1A1-Ile462Val had a minimum prediction error of 31% (P 〈 0.001) and a maximum CVC of 4.40 (P = 0.086). The MDR method seems promising, because it provides a limited number of statistically stable interactions; however, the biological interpretation remains to be understood
    Type of Publication: Journal article published
    PubMed ID: 16956909
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