Piet A van den Brandt

Maastricht Universitair Medisch Centrum, Maestricht, Limburg, Netherlands

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Publications (459)2460.61 Total impact

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    ABSTRACT: Group-based trajectory modelling is a model-based clustering technique applied for the identification of latent patterns of temporal changes. Despite its manifold applications in clinical and health sciences, potential problems of the model selection procedure are often overlooked. The choice of the number of latent trajectories (class-enumeration), for instance, is to a large degree based on statistical criteria that are not fail-safe. Moreover, the process as a whole is not transparent. To facilitate class enumeration, we introduce a graphical summary display of several fit and model adequacy criteria, the fit-criteria assessment plot. An R-code that accepts universal data input is presented. The programme condenses relevant group-based trajectory modelling output information of model fit indices in automated graphical displays. Examples based on real and simulated data are provided to illustrate, assess and validate fit-criteria assessment plot's utility. Fit-criteria assessment plot provides an overview of fit criteria on a single page, placing users in an informed position to make a decision. Fit-criteria assessment plot does not automatically select the most appropriate model but eases the model assessment procedure. Fit-criteria assessment plot is an exploratory, visualisation tool that can be employed to assist decisions in the initial and decisive phase of group-based trajectory modelling analysis. Considering group-based trajectory modelling's widespread resonance in medical and epidemiological sciences, a more comprehensive, easily interpretable and transparent display of the iterative process of class enumeration may foster group-based trajectory modelling's adequate use. © The Author(s) 2015.
    Statistical Methods in Medical Research 08/2015; DOI:10.1177/0962280215598665 · 2.96 Impact Factor
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    ABSTRACT: Vitamins A, C, and E and folate have anticarcinogenic properties and thus might protect against cancer. Few known modifiable risk factors for ovarian cancer exist. We examined the associations between dietary and total (food and supplemental) vitamin intake and the risk of invasive epithelial ovarian cancer. The primary data from 10 prospective cohort studies in North America and Europe were analyzed. Vitamin intakes were estimated from validated food frequency questionnaires in each study. Study-specific relative risks (RRs) were estimated using the Cox proportional hazards model and then combined using a random-effects model. Among 501,857 women, 1,973 cases of ovarian cancer occurred over a median follow-up period of 7-16 years across studies. Dietary and total intakes of each vitamin were not significantly associated with ovarian cancer risk. The pooled multivariate RRs [95 % confidence intervals (CIs)] for incremental increases in total intake of each vitamin were 1.02 (0.97-1.07) for vitamin A (increment: 1,300 mcg/day), 1.01 (0.99-1.04) for vitamin C (400 mg/day), 1.02 (0.97-1.06) for vitamin E (130 mg/day), and 1.01 (0.96-1.07) for folate (250 mcg/day). Multivitamin use (vs. nonuse) was not associated with ovarian cancer risk (pooled multivariate RR = 1.00, 95 % CI 0.89-1.12). Associations did not vary substantially by study, or by subgroups of the population. Greater vitamin intakes were associated with modestly higher risks of endometrioid tumors (n = 156 cases), but not with other histological types. These results suggest that consumption of vitamins A, C, and E and folate during adulthood does not play a major role in ovarian cancer risk.
    Cancer Causes and Control 07/2015; 26(9). DOI:10.1007/s10552-015-0626-0 · 2.96 Impact Factor
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    ABSTRACT: Head and neck cancer (HNC) is the seventh most-common type of cancer worldwide. Evidence regarding the potential protective effect of vitamins and carotenoids on HNC is limited and mostly based on case-control studies. We evaluated the association of intake of dietary vitamins C and E (including supplementation) and the most-common carotenoids (α-carotene, β-carotene, lutein plus zeaxanthin, lycopene, and β-cryptoxanthin) and risk on HNC and HNC subtypes in a large prospective study. The Netherlands Cohort Study included 120,852 participants. For efficiency reasons, a case-cohort design was used. At baseline in 1986, participants completed a food-frequency questionnaire. A subcohort was randomly selected from the total cohort. After 20.3 y of follow-up, 3898 subcohort members and 415 HNC cases [131 oral cavity cancer (OCCs), 88 oro-/hypopharyngeal cancer (OHPs), and 193 laryngeal cancer cases] were available for analysis. Rate ratios and 95% CIs for highest (quartile 4) vs. lowest (quartile 1) quartiles of vitamin and carotenoid intake were estimated by using the Cox proportional hazards model. A strong inverse association was shown between vitamin C and HNC overall (multivariable-adjusted rate ratio for quartile 4 vs. quartile 1: 0.39; 95% CI: 0.23, 0.66; P-trend < 0.001), OCC (multivariable-adjusted rate ratio for quartile 4 vs. quartile 1: 0.35; 95% CI: 0.16, 0.77; P-trend < 0.05), and OHPC (multivariable-adjusted rate ratio for quartile 4 vs. quartile 1: 0.29; 95% CI: 0.12, 0.67; P-trend < 0.01). No statistically significant results were shown for vitamin E, α-carotene, β-carotene, lycopene, and lutein plus zeaxanthin. The association of vitamin E and HNC was modified by alcohol status (P-interaction = 0.003) with lower risks in alcohol abstainers. With this study, we show an inverse association between intake of vitamin C and the incidence of HNC and HNC-subtypes. Future research is recommended to investigate the underlying mechanisms and to confirm our results, which may be promising for the prevention of HNC. © 2015 American Society for Nutrition.
    American Journal of Clinical Nutrition 07/2015; DOI:10.3945/ajcn.114.106096 · 6.92 Impact Factor
  • Piet A van den Brandt · Leo J Schouten
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    ABSTRACT: Nut intake has been associated with lower mortality, but few studies have investigated causes of death other than cardiovascular disease, and dose-response relationships remain unclear. We investigated the relationship of nut (tree nut, peanut) and peanut butter intake with overall and cause-specific mortality. In the Netherlands Cohort Study, 120 852 men and women aged 55-69 years provided information on dietary and lifestyle habits in 1986. Mortality follow-up until 1996 consisted of linkage to Statistics Netherlands. Multivariate case-cohort analyses were based on 8823 deaths and 3202 subcohort members with complete data on nuts and potential confounders. We also conducted meta-analyses of our results with those published from other cohort studies. Total nut intake was related to lower overall and cause-specific mortality (cancer, diabetes, cardiovascular, respiratory, neurodegenerative diseases, other causes) in men and women. When comparing those consuming 0.1-<5, 5-<10 and 10+ g nuts/day with non-consumers, multivariable hazard ratios for total mortality were 0.88, 0.74 and 0.77 [95% confidence interval (CI), 0.66-0.89], respectively (Ptrend = 0.003). Cause-specific hazard ratios comparing 10+ vs 0 g/day varied from 0.56 for neurodegenerative to 0.83 for cardiovascular disease mortality. Restricted cubic splines showed nonlinear dose-response relationships with mortality. Peanuts and tree nuts were inversely related to mortality, whereas peanut butter was not. In meta-analyses, summary hazard ratios for highest vs lowest nut consumption were 0.85 for cancer, and 0.71 for respiratory mortality. Nut intake was related to lower overall and cause-specific mortality, with evidence for nonlinear dose-response relationships. Peanut butter was not related to mortality. © The Author 2015; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.
    International Journal of Epidemiology 06/2015; DOI:10.1093/ije/dyv039 · 9.20 Impact Factor
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    ABSTRACT: We aimed to estimate the proportion of Dutch postmenopausal breast cancer cases in 2010 that is attributable to lifestyle-related risk factors. We calculated population attributable fractions (PAFs) of potentially modifiable risk factors for postmenopausal breast cancer in Dutch women aged >50 in 2010. First, age-specific PAFs were calculated for each risk factor, based on their relative risks for postmenopausal breast cancer (from meta-analyses) and age-specific prevalence in the population (from national surveys) around the year 2000, assuming a latency period of 10 years. To obtain the overall PAF, age-specific PAFs were summed in a weighted manner, using the age-specific breast cancer incidence rates (2010) as weights. 95 % confidence intervals for PAF estimates were derived by Monte Carlo simulations. Of Dutch women >40 years, in 2000, 51 % were overweight/obese, 55 % physically inactive (<5 days/week 30 min activity), 75 % regularly consumed alcohol, 42 % ever smoked cigarettes and 79 % had a low-fibre intake (<3.4 g/1000 kJ/day). These factors combined had a PAF of 25.7 % (95 % CI 24.2-27.2), corresponding to 2,665 Dutch postmenopausal breast cancer cases in 2010. PAFs were 8.8 % (95 % CI 6.3-11.3) for overweight/obesity, 6.6 % (95 % CI 5.2-8.0) for alcohol consumption, 5.5 % (95 % CI 4.0-7.0) for physical inactivity, 4.6 % (95 % CI 3.3-6.0) for smoking and 3.2 % (95 % CI 1.6-4.8) for low-fibre intake. Our findings imply that modifiable risk factors are jointly responsible for approximately one out of four Dutch postmenopausal breast cancer cases. This suggests that incidence rates can be lowered substantially by living a more healthy lifestyle.
    Breast Cancer Research and Treatment 06/2015; DOI:10.1007/s10549-015-3447-7 · 4.20 Impact Factor
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    ABSTRACT: Emerging evidence suggests that light physical activity (LPA), besides moderate-to-vigorous physical activity (MVPA), may beneficially influence physical functioning of colorectal cancer survivors, but its relation with other health-related outcomes is unknown. We applied a biopsychosocial approach to investigate independent associations between self-reported LPA, MVPA and multiple health-related quality of life (HRQoL) outcomes in 2-10y post-diagnosis colorectal cancer survivors. Stage I-III colorectal cancer survivors diagnosed between 2002 and 2010 at Maastricht University Medical Center+, the Netherlands, were included in a cross-sectional study (n = 151). Time spent in LPA and MVPA (hours·week), and HRQoL outcome scores (0-100 points) were assessed by validated questionnaires. Median time spent in LPA and MVPA was 10.0 (interquartile range, 2.0-22.0) and 8.7 hours·week (4.5-15.0), respectively. In multivariable linear regression models, both LPA and MVPA were significantly and independently associated with higher physical functioning (mean difference [MD] between highest and lowest quartile, 10.2; 95% CI, 0.2 to 20.3; and 14.5; 5.1 to 23.9, respectively; both P-trend<0.05). Additionally, LPA was significantly associated with higher role functioning (MD, 19.5; 95% CI, 6.9 to 32.1; P-trend<0.01) and lower disability (MD, -9.9; 95% CI, -17.8 to -1.9; P-trend=0.02), independent from MVPA. Subgroup analyses showed that beneficial associations between LPA and HRQoL were mainly observed in women and participants with multiple comorbidities. Self-reported LPA, besides MVPA, was beneficially associated with multiple HRQoL outcomes in colorectal cancer survivors, especially in women and survivors with multiple comorbidities. Prospective studies are warranted to establish whether LPA is a suitable target for personalized lifestyle interventions to improve the HRQoL of colorectal cancer survivors.
    Medicine and science in sports and exercise 05/2015; DOI:10.1249/MSS.0000000000000698 · 4.46 Impact Factor
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    ABSTRACT: Disease classification system increasingly incorporates information on pathogenic mechanisms to predict clinical outcomes and response to therapy and intervention. Technological advancements to interrogate omics (genomics, epigenomics, transcriptomics, proteomics, metabolomics, metagenomics, interactomics, etc.) provide widely open opportunities in population-based research. Molecular pathological epidemiology (MPE) represents integrative science of molecular pathology and epidemiology. This unified paradigm requires multidisciplinary collaboration between pathology, epidemiology, biostatistics, bioinformatics, and computational biology. Integration of these fields enables better understanding of etiologic heterogeneity, disease continuum, causal inference, and the impact of environment, diet, lifestyle, host factors (including genetics and immunity), and their interactions on disease evolution. Hence, the Second International MPE Meeting was held in Boston in December 2014, with aims to: (1) develop conceptual and practical frameworks; (2) cultivate and expand opportunities; (3) address challenges; and (4) initiate the effort of specifying guidelines for MPE. The meeting mainly consisted of presentations of method developments and recent data in various malignant neoplasms and tumors (breast, prostate, ovarian and colorectal cancers, renal cell carcinoma, lymphoma, and leukemia), followed by open discussion sessions on challenges and future plans. In particular, we recognized need for efforts to further develop statistical methodologies. This meeting provided an unprecedented opportunity for interdisciplinary collaboration, consistent with the purposes of the Big Data to Knowledge, Genetic Associations and Mechanisms in Oncology, and Precision Medicine Initiative of the US National Institute of Health. The MPE meeting series can help advance transdisciplinary population science and optimize training and education systems for twenty-first century medicine and public health.
    Cancer Causes and Control 05/2015; 26(7). DOI:10.1007/s10552-015-0596-2 · 2.96 Impact Factor
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    ABSTRACT: Occupational exposures may be associated with non-vascular dementia. We analyzed the effects of occupational exposures to solvents, pesticides, metals, extremely low frequency magnetic fields (ELF-MF), electrical shocks, and diesel motor exhaust on non-vascular dementia related mortality in the Netherlands Cohort Study (NLCS). Exposures were assigned using job-exposure matrices. After 17.3 years of follow-up, 682 male and 870 female cases were available. Analyses were performed using Cox regression. Occupational exposure to metals, chlorinated solvents and ELF-MF showed positive associations with non-vascular dementia among men, which seemed driven by metals (hazard ratio ever high vs. background exposure: 1.35 [0.98-1.86]). Pesticide exposure showed statistically significant, inverse associations with non-vascular dementia among men. We found no associations for shocks, aromatic solvents, and diesel motor exhaust. Consistent positive associations were found between occupational exposure to metals and non-vascular dementia. The finding on pesticides is not supported in the overall literature. Am. J. Ind. Med. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
    American Journal of Industrial Medicine 05/2015; 58(6). DOI:10.1002/ajim.22462 · 1.59 Impact Factor
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    ABSTRACT: In this era of molecular diagnostics, prediction of clear-cell renal cell cancer (ccRCC) survival requires optimization, as current prognostic markers fail to determine individual patient outcome. Epigenetic events are promising molecular markers. Promoter CpG island methylation of cysteine dioxygenase type 1 (CDO1), which was identified as prognostic marker for breast cancer, is studied as potential marker for ccRCC survival. We collected primary tissues of 365 ccRCC cases identified within the prospective Netherlands Cohort Study (NLCS). In this population-based series, CDO1 promoter methylation was observed in 124 of 324 (38.3%) patients with successful methylation-specific PCR analysis. Kaplan-Meier curves and Wilcoxon tests were used to evaluate 10-year ccRCC-specific survival. Cox regression analysis was used to obtain crude and multivariate hazard ratios (HR) and 95% confidence intervals (CI). The relative prognostic value of multivariate models with and without CDO1 promoter methylation was compared using Likelihood-Ratio tests. Patients with CDO1 promoter methylation have a significantly poorer survival than those without (Wilcoxon P=0.006). Differences in survival were independent of other prognostic factors, including age and sex (HR(95%CI)=1.66(1.12-2.45)) and TNM stage, tumor size and Fuhrman grade (HR(95%CI)=1.89(1.25-2.85)). Multivariate models performed better with than without CDO1 promoter methylation status (Likelihood-Ratio P=0.003). Survival curves were validated in an independent series of 280 ccRCC cases from the Cancer Genome Atlas (TCGA; Wilcoxon P<0.001). CDO1 promoter methylation may not substitute common prognostic makers to predict ccRCC survival, but offers additional, relevant prognostic information, indicating that it could be a novel molecular marker to determine ccRCC prognosis. Copyright © 2015, American Association for Cancer Research.
    Clinical Cancer Research 04/2015; DOI:10.1158/1078-0432.CCR-14-2049 · 8.19 Impact Factor
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    ABSTRACT: The International Agency for Research on Cancer (IARC) recently declared air pollution carcinogenic to humans. However, no study of air pollution and lung cancer to date has incorporated adjustment for exposure measurement error, and few have examined specific histological subtypes. Assess the association of air pollution and incident lung cancer in the Netherlands Cohort Study on Diet and Cancer and the impact of measurement error on these associations. The cohort was followed 1986-2003 and 3,355 incident cases were identified. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals, for long-term exposures to NO2, black smoke (BS), PM2.5, and measures of roadway proximity and traffic volume, adjusted for potential confounders. Information from a previous validation study was used to correct the effect estimates for measurement error. We observed elevated risks of incident lung cancer with exposures to BS (HR=1.16, 95% CI: 1.02, 1.32, per 10 µg/m(3)), NO2 (HR=1.29, 95% CI: 1.08, 1.54, per 30 µg/m(3)), PM2.5 (HR=1.17, 95% CI: 0.93, 1.47, per 10 µg/m(3)), and with measures of traffic at the baseline address. The exposures were positively associated with all lung cancer subtypes. After adjustment for measurement error, the HRs increased and the 95% CIs widened (HR=1.19 (95% CI: 1.02, 1.39) for BS and HR=1.37 (95% CI: 0.86, 2.17) for PM2.5). These findings add support to a growing body of literature on the effects of air pollution on lung cancer. In addition, they highlight variation in measurement error by pollutant and support the implementation of measurement error corrections when possible.
    Environmental Health Perspectives 03/2015; DOI:10.1289/ehp.1408762 · 7.98 Impact Factor
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    ABSTRACT: We investigated the association between six occupational exposures (ie, pesticides, solvents, metals, diesel motor emissions (DME), extremely low frequency magnetic fields (ELF-MF) and electric shocks) and Parkinson's disease (PD) mortality in a large population-based prospective cohort study. The Netherlands Cohort Study on diet and cancer enrolled 58 279 men and 62 573 women aged 55-69 years in 1986. Participants were followed up for cause-specific mortality over 17.3 years, until December 2003, resulting in 402 male and 207 female PD deaths. Following a case-cohort design, a subcohort of 5 000 participants was randomly sampled from the complete cohort. Information on occupational history and potential confounders was collected at baseline. Job-exposure matrices were applied to assign occupational exposures. Associations with PD mortality were evaluated using Cox regression. Among men, elevated HRs were observed for exposure to pesticides (eg, ever high exposed, HR 1.27, 95% CI 0.86 to 1.88) and ever high exposed to ELF-MF (HR 1.54, 95% CI 1.00 to 2.36). No association with exposure duration or trend in cumulative exposure was observed for any of the occupational exposures. Results among women were unstable due to small numbers of high-exposed women. Associations with PD mortality were observed for occupational exposure to pesticides and ELF-MF. However, the weight given to these findings is limited by the absence of a monotonic trend with either duration or cumulative exposure. No associations were found between PD mortality and occupational exposure to solvents, metals, DME or electric shocks. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
    Occupational and Environmental Medicine 02/2015; 72(6). DOI:10.1136/oemed-2014-102209 · 3.23 Impact Factor
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    ABSTRACT: Background: The etiology of male breast cancer is poorly understood, partly due to its relative rarity. Although tobacco and alcohol exposures are known carcinogens, their association with male breast cancer risk remains ill-defined. Methods: The Male Breast Cancer Pooling Project consortium provided 2,378 cases and 51,959 controls for analysis from 10 case-control and 10 cohort studies. Individual participant data were harmonized and pooled. Unconditional logistic regression was used to estimate study design-specific (case-control/cohort) odds ratios (OR) and 95% confidence intervals (CI), which were then combined using fixed effects meta-analysis. Results: Cigarette smoking status, smoking pack-years, duration, intensity, and age at initiation were not associated with male breast cancer risk. Relations with cigar and pipe smoking, tobacco chewing, and snuff use were also null. Recent alcohol consumption and average grams of alcohol consumed per day were also not associated with risk; only one sub-analysis of very high recent alcohol consumption (>60 grams/day) was tentatively associated with male breast cancer (ORunexposed referent=1.29, 95%CI:0.97-1.71; OR>0-<7 g/day referent=1.36, 95%CI:1.04-1.77). Specific alcoholic beverage types were not associated with male breast cancer. Relations were not altered when stratified by age or body mass index. Conclusions: In this analysis of the Male Breast Cancer Pooling Project we found little evidence that tobacco and alcohol exposures were associated with risk of male breast cancer. Impact: Tobacco and alcohol do not appear to be carcinogenic for male breast cancer. Future studies should aim to assess these exposures in relation to subtypes of male breast cancer. Copyright © 2014, American Association for Cancer Research.
    Cancer Epidemiology Biomarkers & Prevention 12/2014; 24(3). DOI:10.1158/1055-9965.EPI-14-1009 · 4.32 Impact Factor
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    ABSTRACT: Nails contain genomic DNA that can be used for genetic analyses, which is attractive for large epidemiologic studies that have collected or are planning to collect nail clippings. Study participants will more readily participate in a study when asked to provide nail samples than when asked to provide a blood sample. In addition, nails are easy and cheap to obtain and store compared with other tissues. We describe our findings on toenail DNA in terms of yield, quality, genotyping a limited set of SNPs with the Sequenom MassARRAY iPLEX platform and high-density genotyping with the Illumina HumanCytoSNP_FFPE-12 DNA array (>262,000 markers). We discuss our findings together with other studies on nail DNA and we compare nails and other frequently used tissue samples as DNA sources. Although nail DNA is considerably degraded, genotyping a limited set of SNPs with the Sequenom MassARRAY iPLEX platform (average sample call rate, 97.1%) and high-density genotyping with the Illumina HumanCytoSNP_FFPE chip (average sample call rate, 93.8%) were successful. Nails are a suitable source of DNA for genotyping in large-scale epidemiologic studies, provided that methods are used that are suitable or optimized for degraded DNA. For genotyping through (next generation) sequencing where DNA degradation is less of an issue, nails may be an even more attractive DNA source, because it surpasses other sources in terms of ease and costs of obtaining and storing the samples. It is worthwhile to consider nails as a source of DNA for genotyping in large-scale epidemiologic studies. See all the articles in this CEBP Focus section, "Biomarkers, Biospecimens, and New Technologies in Molecular Epidemiology." Cancer Epidemiol Biomarkers Prev; 23(12); 2703-12. ©2014 AACR. ©2014 American Association for Cancer Research.
    Cancer Epidemiology Biomarkers & Prevention 12/2014; 23(12):2703-12. DOI:10.1158/1055-9965.EPI-14-0552 · 4.32 Impact Factor
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    ABSTRACT: The evidence for an association between occupational asbestos exposure and esophageal, gastric and colorectal cancer is limited. We studied this association specifically addressing risk differences between relatively low and high exposure, risk associated with cancer subtypes, the influence of potential confounders, and the interaction between asbestos and smoking in relation to cancer risk. Using the Netherlands Cohort Study (n=58279 men, aged 55-69 years at baseline), asbestos exposure was estimated by linkage to a job-exposure matrix. After 17.3 years of follow-up, 187 esophageal, 486 gastric, and 1724 colorectal cancer cases were available for analysis. The models adjusted for age and family history of cancer showed that mainly (prolonged) exposure to high levels of asbestos was statistically significantly associated with risk of esophageal adenocarcinoma (EAC), total and distal colon cancer, and rectal cancer. For overall gastric cancer and gastric non-cardia adenocarcinoma (GNCA), also exposure to lower levels of asbestos was associated. Additional adjustment for lifestyle confounders, especially smoking status, yielded non-significant associations with overall gastric cancer and GNCA in the multivariable-adjusted model, except for the prolonged highly exposed subjects (tertile 3 vs. never: HR 2.67, 95%CI:1.11-6.44 and HR 3.35, 95%CI:1.33-8.44, respectively). No statistically significant additive or multiplicative interaction between asbestos and smoking was observed for any of the studied cancers. This prospective population-based study showed that (prolonged) high asbestos exposure was associated with overall gastric cancer, EAC, GNCA, total and distal colon cancer, and rectal cancer. © 2014 Wiley Periodicals, Inc.
    International Journal of Cancer 10/2014; 135(8). DOI:10.1002/ijc.28817 · 5.01 Impact Factor
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    ABSTRACT: Background: Increased oxidative stress has been linked to prostate cancer (PrCa). We investigated oxidative stress-related genetic variants in relation to advanced PrCa risk and examined potential interactions with pro- and antioxidant exposures. Methods: A case-cohort analysis was conducted in the prospective Netherlands Cohort Study, which included 58,279 men aged 55-69 years. Cohort members completed a baseline questionnaire and provided toenail clippings, which were used to isolate DNA. Advanced PrCa cases were identified during 17.3 years of follow-up. The analysis included 14 genetic variants and 11 exposures. Cox regression models were used for analysis and false discovery rate (FDR) Q-values were calculated. Results: Complete genotyping data were available for 952 cases and 1,798 subcohort members. CAT rs1001179 was associated with stage III/IV and stage IV PrCa risk, with HRs per minor allele of 1.16 (95% CI: 1.01-1.33; P=0.032) and 1.25 (95% CI: 1.07-1.46; P=0.006), respectively. We tested 151 gene-environment interactions in relation to both stage III/IV and IV PrCa risk. Seven interactions were statistically significant after adjusting for multiple testing (FDR Q-value <0.20); for stage III/IV PrCa these involved intake of β-carotene (GPX1 rs17650792, hOGG1 rs1052133) and heme iron (GPX1 rs1800668 and rs3448), and for stage IV PrCa these involved intake of catechin (SOD2 rs4880) and heme iron (hOGG1 rs1052133, SOD1 rs10432782). Conclusion: This study of advanced PrCa risk showed a marginal association with a CAT polymorphism and seven novel gene-environment interactions in the oxidative stress pathway. Impact: Oxidative stress-related genes and exposures may have a joint effect on advanced PrCa.
    Cancer Epidemiology Biomarkers & Prevention 10/2014; 24(1). DOI:10.1158/1055-9965.EPI-14-0968 · 4.32 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):2198-2198. DOI:10.1158/1538-7445.AM2014-2198 · 9.28 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):1272-1272. DOI:10.1158/1538-7445.AM2014-1272 · 9.28 Impact Factor
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    ABSTRACT: There is limited prospective data on the relationship between consumption of vegetables and fruits and the risk of head-neck cancer (HNC) subtypes (i.e., oral cavity cancer (OCC), oro-/hypopharyngeal cancer (OHPC) and laryngeal cancer (LC)). Therefore, we investigated these associations within the Netherlands Cohort Study, in which 120,852 participants completed a 150-item food frequency questionnaire at baseline in 1986. After 20.3 years of follow-up, 415 cases of HNC (131 OCC, 88 OHPC, 3 oral cavity/pharynx unspecified or overlapping and 193 LC) and 3,898 subcohort members were available for case-cohort analysis using Cox proportional hazards models. Total vegetable and fruit consumption was inversely associated with risk of HNC overall (multivariable-adjusted rate ratios for highest vs. lowest quartile: 0.61, 95% confidence interval (CI) 0.44-0.85, P trend 0.002) and all HNC subtypes, with the strongest associations for OCC. Total vegetable intake and total fruit intake were also associated with a decreased risk of HNC overall and HNC subtypes. No significant interaction was found between vegetable and fruit intake and alcohol consumption or cigarette smoking. In conclusion, in this large-scale cohort study, consumption of vegetables and fruits was associated with a decreased risk of HNC overall and all subtypes. Consumption of vegetables and fruits (or of specific groups of them) may protect against HNC and its subtypes. © 2014 Wiley Periodicals, Inc.
    International Journal of Cancer 10/2014; DOI:10.1002/ijc.29219 · 5.01 Impact Factor
  • Cancer Research 10/2014; 74(19 Supplement):5060-5060. DOI:10.1158/1538-7445.AM2014-5060 · 9.28 Impact Factor
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    ABSTRACT: The following, from the 12th OESO World Conference: Cancers of the Esophagus, includes commentaries on macronutrients, dietary patterns, and risk of adenocarcinoma in Barrett's esophagus; micronutrients, trace elements, and risk of Barrett's esophagus and esophageal adenocarcinoma; the role of mate consumption in the development of squamous cell carcinoma; the relationship between energy excess and development of esophageal adenocarcinoma; and the nutritional management of the esophageal cancer patient.
    Annals of the New York Academy of Sciences 09/2014; 1325(1). DOI:10.1111/nyas.12528 · 4.31 Impact Factor

Publication Stats

22k Citations
2,460.61 Total Impact Points


  • 1997–2015
    • Maastricht Universitair Medisch Centrum
      • Central Diagnostic Laboratory
      Maestricht, Limburg, Netherlands
  • 1990–2015
    • Maastricht University
      • • Department of Epidemiology
      • • GROW School for Oncology & Developmental Biology
      • • CAPHRI School for Public Health and Primary Care
      Maestricht, Limburg, Netherlands
  • 2003–2013
    • Universiteit Utrecht
      • Division of Environmental Epidemiology
      Utrecht, Utrecht, Netherlands
  • 2011
    • Yale University
      New Haven, Connecticut, United States
  • 2007
    • Institut Marqués, Spain, Barcelona
      Barcino, Catalonia, Spain
  • 2005
    • VU University Medical Center
      Amsterdamo, North Holland, Netherlands
  • 2004–2005
    • University of Toronto
      Toronto, Ontario, Canada
    • CUNY Graduate Center
      New York City, New York, United States
  • 1998–2004
    • Harvard Medical School
      • • Department of Medicine
      • • Division of Nutrition
      Boston, MA, United States
  • 1988–2002
    • TNO
      Delft, South Holland, Netherlands
  • 2001
    • Beverly Hospital, Boston MA
      Beverly, Massachusetts, United States