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Articles by P Boffetta
Total Records ( 5 ) for P Boffetta
  B Hoeft , J Linseisen , L Beckmann , K Muller Decker , F Canzian , A Husing , R Kaaks , U Vogel , M. U Jakobsen , K Overvad , R. D Hansen , S Knuppel , H Boeing , A Trichopoulou , Y Koumantaki , D Trichopoulos , F Berrino , D Palli , S Panico , R Tumino , H.B Bueno de Mesquita , F. J.B van Duijnhoven , C. H van Gils , P. H Peeters , V Dumeaux , E Lund , J. M Huerta Castano , X Munoz , L Rodriguez , A Barricarte , J Manjer , K Jirstrom , B Van Guelpen , G Hallmans , E. A Spencer , F. L Crowe , K. T Khaw , N Wareham , S Morois , M. C Boutron Ruault , F Clavel Chapelon , V Chajes , M Jenab , P Boffetta , P Vineis , T Mouw , T Norat , E Riboli and A. Nieters

Colorectal cancer (CRC) is the third most common malignant tumor and the fourth leading cause of cancer death worldwide. The crucial role of fatty acids for a number of important biological processes suggests a more in-depth analysis of inter-individual differences in fatty acid metabolizing genes as contributing factor to colon carcinogenesis. We examined the association between genetic variability in 43 fatty acid metabolism-related genes and colorectal risk in 1225 CRC cases and 2032 controls participating in the European Prospective Investigation into Cancer and Nutrition study. Three hundred and ninety two single-nucleotide polymorphisms were selected using pairwise tagging with an r2 cutoff of 0.8 and a minor allele frequency of >5%. Conditional logistic regression models were used to estimate odds ratios and corresponding 95% confidence intervals. Haplotype analysis was performed using a generalized linear model framework. On the genotype level, hydroxyprostaglandin dehydrogenase 15-(NAD) (HPGD), phospholipase A2 group VI (PLA2G6) and transient receptor potential vanilloid 3 were associated with higher risk for CRC, whereas prostaglandin E receptor 2 (PTGER2) was associated with lower CRC risk. A significant inverse association (P < 0.006) was found for PTGER2 GGG haplotype, whereas HPGD AGGAG and PLA2G3 CT haplotypes were significantly (P < 0.001 and P = 0.003, respectively) associated with higher risk of CRC. Based on these data, we present for the first time the association of HPGD variants with CRC risk. Our results support the key role of prostanoid signaling in colon carcinogenesis and suggest a relevance of genetic variation in fatty acid metabolism-related genes and CRC risk.

  G Andreotti , P Boffetta , P. S Rosenberg , S. I Berndt , S Karami , I Menashe , M Yeager , S. J Chanock , D Zaridze , V Matteev , V Janout , H Kollarova , V Bencko , M Navratilova , N Szeszenia Dabrowska , D Mates , N Rothman , P Brennan , W. H Chow and L. E. Moore

Hypertension is a known risk factor for renal cell carcinoma (RCC), although the underlying biological mechanisms of its action are unknown. To clarify the role of hypertension in RCC, we examined the risk of RCC in relation to 142 single-nucleotide polymorphisms (SNPs) in eight genes having a role in blood pressure control. We analyzed 777 incident and histologically confirmed RCC cases and 1035 controls who completed an in-person interview as part of a multi-center, hospital-based case–control study in Central Europe. Genotyping was conducted with an Illumina® GoldenGate® Oligo Pool All assay using germ line DNA. Of the eight genes examined, AGT (angiotensinogen) was most strongly associated with RCC (minimum P-value permutation test = 0.02). Of the 17 AGT tagging SNPs considered, associations were strongest for rs1326889 [odds ratio (OR) = 1.35, 95% confidence interval (CI) = 1.15–1.58] and rs2493137 (OR = 1.31, 95% CI = 1.12–1.54), which are located in the promoter. Stratified analysis revealed that the effects of the AGT SNPs were statistically significant in participants with hypertension or high body mass index (BMI) (≥25 kg/m2), but not in subjects without hypertension and with a normal BMI (<25 kg/m2). Also, haplotypes with risk-conferring alleles of markers located in the promoter and intron 1 regions of AGT were significantly associated with RCC compared with the common haplotype in subjects with hypertension or high BMI (global P = 0.003). Our findings suggest that common genetic variants of AGT, particularly those in the promoter, increase RCC risk among subjects who are hypertensive or overweight.

  T Truong , W Sauter , J. D McKay , H. D Hosgood , C Gallagher , C. I Amos , M Spitz , J Muscat , P Lazarus , T Illig , H. E Wichmann , H Bickeboller , A Risch , H Dienemann , Z. F Zhang , B. P Naeim , P Yang , S Zienolddiny , A Haugen , L Le Marchand , Y. C Hong , J. H Kim , E. J Duell , A. S Andrew , C Kiyohara , H Shen , K Matsuo , T Suzuki , A Seow , D. P. K Ng , Q Lan , D Zaridze , N Szeszenia Dabrowska , J Lissowska , P Rudnai , E Fabianova , V Constantinescu , V Bencko , L Foretova , V Janout , N. E Caporaso , D Albanes , M Thun , M. T Landi , J Trubicka , M Lener , J Lubinski , Wang EPIC lung , A Chabrier , P Boffetta , P Brennan and R. J. Hung

Background. Analysis of candidate genes in individual studies has had only limited success in identifying particular gene variants that are conclusively associated with lung cancer risk. In the International Lung Cancer Consortium (ILCCO), we conducted a coordinated genotyping study of 10 common variants selected because of their prior evidence of an association with lung cancer. These variants belonged to candidate genes from different cancer-related pathways including inflammation (IL1B), folate metabolism (MTHFR), regulatory function (AKAP9 and CAMKK1), cell adhesion (SEZL6) and apoptosis (FAS, FASL, TP53, TP53BP1 and BAT3). Methods. Genotype data from 15 ILCCO case–control studies were available for a total of 8431 lung cancer cases and 11 072 controls of European descent and Asian ethnic groups. Unconditional logistic regression was used to model the association between each variant and lung cancer risk. Results. Only the association between a non-synonymous variant of TP53BP1 (rs560191) and lung cancer risk was significant (OR = 0.91, P = 0.002). This association was more striking for squamous cell carcinoma (OR = 0.86, P = 6 x 10–4). No heterogeneity by center, ethnicity, smoking status, age group or sex was observed. In order to confirm this association, we included results for this variant from a set of independent studies (9966 cases/11 722 controls) and we reported similar results. When combining all these studies together, we reported an overall OR = 0.93 (0.89–0.97) (P = 0.001). This association was significant only for squamous cell carcinoma [OR = 0.89 (0.85–0.95), P = 1 x 10–4]. Conclusion. This study suggests that rs560191 is associated to lung cancer risk and further highlights the value of consortia in replicating or refuting published genetic associations.

  P Boffetta , J. K McLaughlin , R. E Tarone and W. J Blot
  No Description
  M Agostini , G Ferro , A Olsson , I Burstyn , F De Vocht , J Hansen , C Funch Lassen , C Johansen , K Kjaerheim , S Langard , I Stucker , W Ahrens , T Behrens , M. L Lindbohm , P Heikkila , D Heederik , L Portengen , J Shaham , P Boffetta and H. Kromhout

Objective: Development of a method for retrospective assessment of exposure to bitumen fume, bitumen condensate, organic vapour, polycyclic aromatic hydrocarbons, and co-exposures to known or suspected lung carcinogens for a nested case–control study of lung cancer mortality among European asphalt workers.

Methods: Company questionnaires and structured questionnaires used in interviews and industry-specific job-exposure matrices (JEMs) were elaborated and applied. Three sources of information were eventually used for exposure assessment and assignment: (i) data obtained in cohort phase, (ii) data from living subjects, next-of-kin, and fellow-workers questionnaires, and (iii) JEMs for bitumen exposure by inhalation and via skin and co-exposures to known or suspected lung carcinogens within and outside cohort companies. Inhalation and dermal exposure estimates for bitumen were adjusted for time trends, time spent in a job, and other determinants of exposure (e.g. oil gravel paving). Clothing patterns, personal protective devices, and personal hygiene were taken into consideration while estimating dermal exposure.

Results: Occupational exposures could be assessed for 433 cases and 1253 controls for relevant time periods. Only 43% of work histories were spent inside original asphalt and construction companies. A total of 95.8% of job periods in cohort companies could be coded at a more detailed level. Imputation of work time and ‘hygienic behaviour’ multipliers was needed for <10% of work history years. Overall, downward trends in exposure were present and differences existed between countries and companies. As expected, correlations were strongest (r > 0.7) among bitumen-related agents, while correlations between coal tar, bitumen-related agents, and established lung carcinogens were weaker (r < 0.4).

Conclusions: A systematic and detailed approach was developed to estimate inhalation and dermal exposure for a nested case–control study among asphalt workers.

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