Piet A van den Brandt

Maastricht Universitair Medisch Centrum, Maestricht, Limburg, Netherlands

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Publications (466)2474.76 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Studies of the role of dietary factors in epithelial ovarian cancer (EOC) development have been limited, and no specific dietary factors have been consistently associated with EOC risk. Objective: We used a nutrient-wide association study approach to systematically test the association between dietary factors and invasive EOC risk while accounting for multiple hypothesis testing by using the false discovery rate and evaluated the findings in an independent cohort. Design: We assessed dietary intake amounts of 28 foods/food groups and 29 nutrients estimated by using dietary questionnaires in the EPIC (European Prospective Investigation into Cancer and Nutrition) study (n = 1095 cases). We selected 4 foods/nutrients that were statistically significantly associated with EOC risk when comparing the extreme quartiles of intake in the EPIC study (false discovery rate = 0.43) and evaluated these factors in the NLCS (Netherlands Cohort Study; n = 383 cases). Cox regression models were used to estimate HRs and 95% CIs. Results: None of the 4 dietary factors that were associated with EOC risk in the EPIC study (cholesterol, polyunsaturated and saturated fat, and bananas) were statistically significantly associated with EOC risk in the NLCS; however, in meta-analysis of the EPIC study and the NLCS, we observed a higher risk of EOC with a high than with a low intake of saturated fat (quartile 4 compared with quartile 1; overall HR: 1.21; 95% CI: 1.04, 1.41). Conclusion: In the meta-analysis of both studies, there was a higher risk of EOC with a high than with a low intake of saturated fat.
    American Journal of Clinical Nutrition 11/2015; DOI:10.3945/ajcn.115.118588 · 6.77 Impact Factor
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    ABSTRACT: Low mitochondrial DNA (mtDNA) copy number in tumors has been associated with worse prognosis in colorectal cancer (CRC). This study further deciphers the role of mtDNA copy number in CRC by comparing mtDNA copy number between healthy, adenoma and carcinoma tissue, by investigating its association according to several clinicopathological characteristics in CRC, and by relating it to CRC-specific survival in CRC patients. A hospital-based series of samples including cancer, adenoma and adjacent histologically normal tissue from primary CRC patients (n=56) and recurrent CRC (n=16) was studied as well as colon mucosa samples from healthy subjects (n=76). Furthermore, mtDNA copy number was assessed in carcinomas of 693 CRC cases identified from the population-based Netherlands Cohort Study (NLCS). MtDNA copy number was significantly lower in carcinoma tissue (p=0.011) and adjacent tissue (p<;0.001) compared to earlier resected adenoma tissue and in primary CRC tissue compared to recurrent CRC tissue (p=0.011). Within both study populations, mtDNA copy number was significantly lower in mutated BRAF (p=0.027 and p=0.006) and in microsatellite unstable (MSI) tumors (p=0.033 and p<0.001) and higher in KRAS mutated tumors (p=0.004). Furthermore, the association between mtDNA and survival seemed to follow an inverse U-shape with the highest HR observed in the second quintile of mtDNA copy number (HR=1.70, 95% C.I.=1.18, 2.44) compared to the first quintile. These results might reflect an association of mtDNA copy number with various malignant processes in cancer cells and warrants further research on tumor energy metabolism in CRC prognosis.
    Carcinogenesis 10/2015; DOI:10.1093/carcin/bgv151 · 5.33 Impact Factor
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    ABSTRACT: Interrelationships between insulin-like growth factors (IGFs), hyperinsulinaemia, diabetes, and colorectal cancer (CRC) indicate involvement of IGFs in colorectal tumorigenesis. We investigated the CRC risk associated with 24 single nucleotide polymorphisms (SNPs) in 9 genes related to the IGF pathway and an IGF1 19-CA repeat polymorphism. Variants were selected from literature and genotyped in toenail DNA from 3,768 subcohort members and 2,580 CRC cases from the Netherlands Cohort Study, which has a case-cohort design (n = 120,852). We used the follow-up period 1986-2002. Eighteen SNPs were unequivocally associated with selected endpoints in the literature and unfavorable alleles were aggregated into a genetic sum score. Cox regression showed that a higher genetic sum score significantly increased CRC risk at all subsites, except the rectum, in men (highest vs. lowest tertile: HR for CRC = 1.36, 95% CI: 1.11, 1.65; P-trend = 0.002). Single SNPs (except the IGF1 SNP rs5742694) were not associated with risk. Models including the total number of IGF1 19-CA repeats showed CRC risk was halved at all subsites in women carrying <38 repeats but not >38 repeats (≤36 versus 38 repeats: HR for CRC = 0.44; 95% CI: 0.33, 0.58; P-trend < 0.001). These findings support a role for variants in IGF-related genes in colorectal tumorigenesis.
    Scientific Reports 09/2015; 5:14126. DOI:10.1038/srep14126 · 5.58 Impact Factor
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    ABSTRACT: Insulin-like growth factors (IGFs) have been associated with growth, body size, physical activity and colorectal cancer (CRC). We hypothesized that variants in IGF-related genes increase the CRC susceptibility associated with a larger body size and a lack of physical activity. We assessed this in The Netherlands Cohort Study. Participants ( n = 120852) completed a baseline questionnaire on diet and cancer. ~75% returned toenail clippings. Using a case-cohort approach and 16.3 years of follow-up, toenail DNA from 3768 subcohort members and 2580 CRC cases was genotyped. We aggregated unfavorable alleles (potentially increasing CRC risk) for 18 single nucleotide polymorphisms in 8 genes into a sum score. The sum score (in tertiles) and an IGF1 19-CA repeat polymorphism (19/19, 19/non-19 and non-19/non-19 repeats) in combination with body size (mostly in tertiles) and (non-)occupational physical activity (>12, 8–12 and <8 kJ/min in the job and >90, >60–90, >30–60 and 30min/day) were analyzed by Cox regression. Increasingly higher hazard ratios (HRs) for CRC were observed for a larger adult body mass index, larger trouser size and tallness in the presence of more unfavorable alleles in men. HRs (95% confidence intervals) for joint effects were 1.55 (1.06–2.25), 1.78 (1.29–2.46) and 1.48 (1.01–2.17), respectively. In women, variant repeat alleles halved CRC risk irrespective of body size and physical activity. Almost no interactions tested significant. To conclude, a larger body size was a CRC risk factor in men in the presence of an accumulation of unfavorable alleles in IGF-related genes, but interactions were generally nonsignificant.
    Carcinogenesis 09/2015; 36(9). DOI:10.1093/carcin/bgv077 · 5.33 Impact Factor
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    ABSTRACT: To study how a vegetarian or low meat diet influences the risk of colorectal cancer compared to a high meat diet, and to assess the explanatory role of factors associated with these diets. In the Netherlands Cohort Study - Meat Investigation Cohort (NLCS-MIC) (cohort of 10,210 individuals including 1040 self-defined vegetarians), subjects completed a baseline questionnaire in 1986, based on which they were classified into vegetarians (n = 635), pescetarians (n = 360), 1 day/week- (n = 1259), 2-5 day/week- (n = 2703), and 6-7 day/week meat consumers (n = 5253). After 20.3 years of follow-up, 437 colorectal cancer cases (307 colon, 92 rectal) were available. A non-significantly decreased risk of CRC for vegetarians, pescetarians, and 1 day/week compared to 6-7 day/week meat consumers was observed (age/sex adjusted Hazard Ratios (HR): 0.73(0.47-1.13), 0.80(0.47-1.39), and 0.72(0.52-1.00), respectively). Most of the differences in HR between these groups could be explained by intake of dietary fiber and soy products. Other (non-)dietary factors characteristic for a vegetarian or low meat diet had negligible individual effects, but attenuated the HRs towards the null when combined. Vegetarians, pescetarians, and 1 day/week meat eaters showed a non-significantly decreased risk of colorectal cancer compared to 6-7 day/week meat consumers, mainly due to differences in dietary pattern other than meat intake.
    Scientific Reports 08/2015; 5:13484. DOI:10.1038/srep13484 · 5.58 Impact Factor
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    ABSTRACT: Breast cancer aetiology may differ by estrogen receptor (ER) status. Associations of alcohol and folate intakes with risk of breast cancer defined by ER status were examined in pooled analyses of the primary data from 20 cohorts. During a maximum of 6-18 years of follow-up of 1 089 273 women, 21 624 ER+ and 5113 ER- breast cancers were identified. Study-specific multivariable relative risks (RRs) were calculated using Cox proportional hazards regression models and then combined using a random-effects model. Alcohol consumption was positively associated with risk of ER+ and ER- breast cancer. The pooled multivariable RRs (95% confidence intervals) comparing ≥ 30 g/d with 0 g/day of alcohol consumption were 1.35 (1.23-1.48) for ER+ and 1.28 (1.10-1.49) for ER- breast cancer (Ptrend ≤ 0.001; Pcommon-effects by ER status: 0.57). Associations were similar for alcohol intake from beer, wine and liquor. The associations with alcohol intake did not vary significantly by total (from foods and supplements) folate intake (Pinteraction ≥ 0.26). Dietary (from foods only) and total folate intakes were not associated with risk of overall, ER+ and ER- breast cancer; pooled multivariable RRs ranged from 0.98 to 1.02 comparing extreme quintiles. Following-up US studies through only the period before mandatory folic acid fortification did not change the results. The alcohol and folate associations did not vary by tumour subtypes defined by progesterone receptor status. Alcohol consumption was positively associated with risk of both ER+ and ER- breast cancer, even among women with high folate intake. Folate intake was not associated with breast cancer risk. © The Author 2015; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.
    International Journal of Epidemiology 08/2015; DOI:10.1093/ije/dyv156 · 9.18 Impact Factor
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    ABSTRACT: DOI 10.1007/s10654-015-0072-z
    Healthy Living: The European Congress of Epidemiology, 2015, Eur J Epidemiol.; 08/2015
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    Sven L Klijn · Matty P Weijenberg · Paul Lemmens · Piet A van den Brandt · Valéria Lima Passos ·
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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 · 4.47 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 · 2.74 Impact Factor
  • Leonie de Munter · Denise He Maasland · Piet A van den Brandt · Bernd Kremer · Leo J Schouten ·
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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; 102(2). DOI:10.3945/ajcn.114.106096 · 6.77 Impact Factor
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    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; 44(3). DOI:10.1093/ije/dyv039 · 9.18 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; 152(1). DOI:10.1007/s10549-015-3447-7 · 3.94 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 · 3.98 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 · 2.74 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 · 1.74 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; 21(15). DOI:10.1158/1078-0432.CCR-14-2049 · 8.72 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; 123(9). 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 · 3.27 Impact Factor
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    ABSTRACT: To calculate the proportion of cancer cases in the Netherlands in 2010 that were attributable to lifestyle factors by using the most recent data. Secondary analysis. Lifestyle risk factors studied were tobacco smoking, alcohol consumption, overweight, lack of physical exercise, and six elements of diet (consumption of vegetables, fruit, processed meat and red meat, and calcium and fibre intake). The lifestyle factors were organised so that the group with the highest risk (e.g. smokers) could be compared with the groups with the lowest risk (e.g. ex-smokers, non-smokers). Cut-off points were in line with Dutch public health messages. We obtained prevalence data on risk factors from national databases. Relative risks for the relationship between lifestyle and cancer were based on the international literature. Incidence and mortality data for cancer in 2010 were obtained through the Netherlands Cancer Registry. We calculated percentages of new cancer cases and deaths for men and women and for each type of cancer individually; these were then summed. We estimated that of the 98,971 newly-diagnosed cases of cancer among persons aged ≥ 20 years in the Netherlands in 2010, 29,938 (30%) were attributable to the above-mentioned lifestyle factors. Smoking was the most important contributory risk factor (19% of all new cancer cases), followed by sub-optimal dietary habits (10%), overweight (4%), alcohol consumption (3%), and lack of physical activity (2%). Of cancer deaths in 2010, an estimated 38% were attributable to lifestyle factors. Projections for 2020 show that lack of exercise and consumption of alcohol and meat will contribute less to the development of cancer while overweight and a reduction in inadequate dietary fibre intake and inadequate fruit and vegetable consumption will contribute more. Almost one-third of all cases of cancer and almost 40% of deaths from cancer can be attributed to a less healthy lifestyle.
    Nederlands tijdschrift voor geneeskunde 12/2014; 159:A8085.
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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 · 4.13 Impact Factor

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  • 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
  • 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
    • CUNY Graduate Center
      New York City, New York, United States
  • 2003
    • Utrecht University
      Utrecht, Utrecht, Netherlands
  • 1998-2002
    • Harvard Medical School
      • Division of Nutrition
      Boston, Massachusetts, United States
  • 2001
    • Beverly Hospital, Boston MA
      Beverly, Massachusetts, United States
  • 1988-2000
    • TNO
      Delft, South Holland, Netherlands