DNA Adducts and Lung Cancer Risk: A Prospective Study

Peluso, Marco; Munnia, Armelle; Hoek, Gerard; Krzyżanowski, Michał; Veglia, Fabrizio; Airoldi, Luisa; Autrup, Herman; Dunning, Alison M.; Garte, Seymour; Hainaut, Pierre; Malaveille, Christian; Gormally, Emmanuelle; Matullo, Giuseppe; Overvad, Kim; Raaschou-Nielsen, Ole; Clavel‐Chapelon, Françoise; Linseisen, Jakob; Boeing, Heiner; Trichopoulou, Antonia; Trichopoulos, Dimitrios; Kaladidi, Anna; Palli, Domenico; Krogh, Vittorio; Tumino, Rosario; Panico, Salvatore; Bueno-De-Mesquita, H. Bas; Peeters, Petra H.; Kumle, Merethe; González, Carlos; Martínez, Carmen; Dorronsoro, Miren; Barricarte, Aurelio; Navarro, Carmen; Quiŕos, J. Ramón; Berglund, Göran; Janzon, Lars; Järvholm, Bengt; Day, Nicholas E.; Key, Tim; Saracci, Rodolfo; Kaaks, Rudolf; Riboli, Elio; Víneis, Paolo

doi:10.1158/0008-5472.can-04-3488

Cited by 106 publications

(103 citation statements)

References 39 publications

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“…12 Therefore, it is not necessarily relevant, at least in causal assessment, to distinguish among single pollutants; rather, they might interact in unpredictable ways. O 3 has been found to damage DNA in 2 epidemiological studies, including the present one, 13,14 but its role is more difficult to assess because of strong negative association with other 2 , 27 vs <27 lg/m 3 for PM10, and 11 vs <11 lg/m 3 for SO 2 (see text).-2 As in footnote 1 but additionally adjusted by BMI, education, intake of fruit and vegetables, intake of meat, intake of alcohol, physical activity.-3 As in footnote 1 but additionally adjusted by cotinine.- 4 As in footnote 1 but additionally adjusted by occupational index (see text).…”

Section: Discussionsupporting

confidence: 49%

Air pollution and risk of lung cancer in a prospective study in Europe

Víneis

Hoek

Krzyżanowski

et al. 2006

Intl Journal of Cancer

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159

105

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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 (65 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 (NO 2 , PM10, SO 2 ) 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 5 1.46, 95% confidence interval, CI, 0.89-2.40).

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Section: Discussionsupporting

confidence: 49%

Air pollution and risk of lung cancer in a prospective study in Europe

Víneis

Hoek

Krzyżanowski

et al. 2006

Intl Journal of Cancer

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159

105

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“…Recent publications have reported associations with biomarkers of environmental exposures in the GENAIR cohorts, including bulky DNA adducts in WBC (12), and biomarkers of genetic susceptibility, such as polymorphisms in genes involved in carcinogen metabolism, detoxification, and DNA repair (17). 32 Here, we have reanalyzed these previously reported data with respect to the presence of mutations in plasma DNA (Table 3).…”

Section: Resultsmentioning

confidence: 99%

“…GENAIR is a case-control study nested within the EPIC cohort, aiming at studying the relationship between some types of cancers and air pollution or environmental tobacco smoke (12). Cases are subjects with bladder, lung, or UADT cancers or leukemia, all newly diagnosed after recruitment.…”

Section: Methodsmentioning

confidence: 99%

TP53 and KRAS2 Mutations in Plasma DNA of Healthy Subjects and Subsequent Cancer Occurrence: A Prospective Study

et al. 2006

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In cancer patients, plasma often contains mutant DNA released by cancer cells. We have assessed the significance of plasma DNA mutations for subsequent cancer development in healthy subjects in a large longitudinal prospective study. The European Prospective Investigation into Cancer and Nutrition study was analyzed with a nested case-control design. Cases were nonsmokers or ex-smokers for >10 years and newly diagnosed with lung, bladder, or upper aerodigestive tract cancers or leukemia accrued after a median follow-up of 6.3 years. Controls were matched 2:1 for follow-up, age, sex, area of recruitment, and smoking status. KRAS2 mutations were detected by mutant-enriched PCR and sequencing (n = 1,098). TP53 mutations were detected by denaturing high-performance liquid chromatography, temporal temperature gradient electrophoresis, and sequencing (n = 550). KRAS2 or TP53 mutations were detected in 13 of 1,098 (1.2%) and 20 of 550 (3.6%) subjects, respectively, 16 of whom developed cancer on average after 18.3 months of follow-up. Among 137 subjects who developed bladder cancer, 5 had KRAS2 mutations [odds ratio (OR), 4.25; 95% confidence interval (95% CI), 1.27-14.15] and 7 had TP53 mutations (OR, 1.81; 95% CI, 0.66-4.97). There was a nonsignificant trend for association between TP53 mutations and bulky adducts in lymphocyte DNA (OR, 2.78; 95% CI,. This is the first report of TP53 or KRAS2 mutations in the plasma of healthy subjects in a prospective study, suggesting that KRAS2 mutation is detectable ahead of bladder cancer diagnosis. TP53 mutation may be associated with environmental exposures. These observations have implications for monitoring early steps of carcinogenesis. (Cancer Res 2006; 66(13): 6871-6)

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“…Neither age nor race was associated with BCR in our study population, but elevated DNA adduct levels had the strongest association with BCR in younger African-American cases. The combination of high adduct levels and younger age has been associated with higher risk of lung (53) and colorectal (54) cancer. Hu et al (50) found lower nucleotide excision repair capacity was a stronger risk for prostate cancer in men younger than 60 years old and that the nucleotide excision repair capacity level was lower in younger cases, suggesting that deficient nucleotide excision repair capacity could contribute to early onset of prostate cancer.…”

Section: Discussionmentioning

confidence: 99%

Polycyclic Aromatic Hydrocarbon–DNA Adducts in Prostate and Biochemical Recurrence after Prostatectomy

Rybicki

Neslund‐Dudas²,

Bock

et al. 2008

Clinical Cancer Research

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Purpose: DNA adduct levels may be influenced by metabolic activity, DNA repair capabilities, and genomic integrity, all of which play a role in cancer progression. Experimental Design: To determine if elevated DNA adducts are a marker for prostate cancer progression, we measured polycyclic aromatic hydrocarbon^DNA adducts by immunohistochemistry in prostate cells of 368 surgical prostate cancer patients treated at the Henry Ford Hospital in Detroit, Michigan, between September 1999 and July 2004. Patients were followed up to 5 years after surgery with relative risk for biochemical recurrence (BCR) estimated with a Cox proportional hazards model that adjusted for standard clinical risk factors. Results: At 1 year of follow-up, patients with adduct levels above the median in tumor cells [hazard ratio (HR), 2.40; 95% confidence interval (95% CI), 1.10-5.27] and nontumor cells (HR, 3.22; 95% CI, 1.40-7.39) had significant increased risk of BCR, but these HRs decreased to 1.12 (95% CI, 0.68-1.83) and 1.46 (95% CI, 0.89-2.41) in tumor and nontumor cells at 5 years postsurgery. When we restricted our analysis to patients with advanced-stage (III+) disease, those with high adduct levels in either tumor (53.5% versus 30.2%; P = 0.07) or nontumor (55.2% versus 28.6%; P = 0.02) cells had BCR rates almost 2-fold higher. In race-stratified analyses, the greatest risk of BCR associated with high adduct levels (in nontumor cells) was for African American patients younger than 60 years old (HR, 3.79; 95% CI, 1.01-14.30). Conclusions: High polycyclic aromatic hydrocarbon^DNA adduct levels in nontumor prostate cells are most strongly associated with BCR between 1 and 2 years after surgery and in patient subsets defined by younger age, advanced tumor stage, and African American race.

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DNA Adducts and Lung Cancer Risk: A Prospective Study

Cited by 106 publications

References 39 publications

Air pollution and risk of lung cancer in a prospective study in Europe

Air pollution and risk of lung cancer in a prospective study in Europe

TP53 and KRAS2 Mutations in Plasma DNA of Healthy Subjects and Subsequent Cancer Occurrence: A Prospective Study

Polycyclic Aromatic Hydrocarbon–DNA Adducts in Prostate and Biochemical Recurrence after Prostatectomy

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