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  1. Beulens JWJ, Fransen HP, Struijk EA, Boer JMA, de Wit GA, Onland-Moret NC, et al.
    Eur J Epidemiol, 2017 04;32(4):317-326.
    PMID: 28409278 DOI: 10.1007/s10654-017-0247-x
    The relation of alcohol consumption with disease burden remains debated partly due to opposite associations with cardiovascular disease (CVD) and cancer. The relation of alcohol consumption with disease burden expressed in disability-adjusted life years (DALYs) summarizes opposing associations of alcohol consumption on chronic diseases. This study aimed to investigate the association of alcohol consumption with chronic disease burden expressed in DALYs based on individual-participant data. The study was a prospective study among 33,066 men and women from the EPIC-NL cohort. At baseline, alcohol consumption was assessed with a validated food-frequency questionnaire. Participants were followed for occurrence of and mortality from chronic diseases and DALYs were calculated. After 12.4 years follow-up, 6647 disease incidences and 1482 deaths were documented, resulting in 68,225 healthy years of life lost (6225 DALYs). Moderate drinkers (women 5-14.9 g/day, men 5-29.9 g/day) had a lower chronic disease burden (mean DALYs -0.27; 95% CI -0.43; -0.11) than light drinkers (0-4.9 g/day), driven by a lower disease burden due to CVD (-0.18: -0.29; -0.06) but not cancer (-0.05: -0.16; 0.06). The associations were most pronounced among older participants (≥50 years; -0.32; -0.53; -0.10) and not observed among younger women (-0.08; -0.43; 0.35), albeit non-significant (pinteraction > 0.14). Substantial drinking (women 15-29.9 g/day, men 30-59.9 g/day) compared to light drinking was not associated with chronic disease burden. Our results show that moderate compared to light alcohol consumption was associated with living approximately 3 months longer in good health. These results were mainly observed among older participants and not seen among younger women.
  2. Fransen HP, Boer JMA, Beulens JWJ, de Wit GA, Bueno-de-Mesquita HB, Hoekstra J, et al.
    Eur J Public Health, 2017 04 01;27(2):274-278.
    PMID: 27744349 DOI: 10.1093/eurpub/ckw190
    Background: : Unhealthy dietary patterns have been associated with other unhealthy lifestyle factors such as smoking and physical inactivity. Whether these associations are similar in high- and low-educated individuals is currently unknown.

    Methods: We used information of the EPIC-NL cohort, a prospective cohort of 39 393 men and women, aged 20-70 years at recruitment. A lifestyle questionnaire and a validated food frequency questionnaire were administered at recruitment (1993-97). Low adherence to a Mediterranean-style diet was used to determine an unhealthy dietary pattern. Lifestyle-related factors included body mass index, waist circumference, smoking status, physical activity level, dietary supplement use and daily breakfast consumption. Multivariate logistic regression analyses were performed for the total population and by strata of educational level.

    Results: In total 30% of the study population had an unhealthy dietary pattern: 39% in the lowest educated group and 20% in the highest educated group. Physical inactivity, a large waist circumference, no dietary supplement use and skipping breakfast were associated with an unhealthy dietary pattern in both low and high educated participants. Among low educated participants, current smokers had a greater odds of an unhealthy diet compared with never smokers: OR 1.42 (95% CI: 1.25; 1.61). This association was not observed in the high educated group.

    Conclusions: Most associations between lifestyle-related factors and unhealthy diet were consistent across educational levels, except for smoking. Only among low educated participants, current smokers reported an unhealthier dietary pattern in comparison to never smokers. These results can be used in the development of targeted health promotion strategies.

  3. Ordóñez-Mena JM, Walter V, Schöttker B, Jenab M, O'Doherty MG, Kee F, et al.
    Ann Oncol, 2018 Feb 01;29(2):472-483.
    PMID: 29244072 DOI: 10.1093/annonc/mdx761
    BACKGROUND: Smoking has been associated with colorectal cancer (CRC) incidence and mortality in previous studies and might also be associated with prognosis after CRC diagnosis. However, current evidence on smoking in association with CRC prognosis is limited.

    PATIENTS AND METHODS: For this individual patient data meta-analysis, sociodemographic and smoking behavior information of 12 414 incident CRC patients (median age at diagnosis: 64.3 years), recruited within 14 prospective cohort studies among previously cancer-free adults, was collected at baseline and harmonized across studies. Vital status and causes of death were collected for a mean follow-up time of 5.1 years following cancer diagnosis. Associations of smoking behavior with overall and CRC-specific survival were evaluated using Cox regression and standard meta-analysis methodology.

    RESULTS: A total of 5229 participants died, 3194 from CRC. Cox regression revealed significant associations between former [hazard ratio (HR) = 1.12; 95 % confidence interval (CI) = 1.04-1.20] and current smoking (HR = 1.29; 95% CI = 1.04-1.60) and poorer overall survival compared with never smoking. Compared with current smoking, smoking cessation was associated with improved overall (HR<10 years = 0.78; 95% CI = 0.69-0.88; HR≥10 years = 0.78; 95% CI = 0.63-0.97) and CRC-specific survival (HR≥10 years = 0.76; 95% CI = 0.67-0.85).

    CONCLUSION: In this large meta-analysis including primary data of incident CRC patients from 14 prospective cohort studies on the association between smoking and CRC prognosis, former and current smoking were associated with poorer CRC prognosis compared with never smoking. Smoking cessation was associated with improved survival when compared with current smokers. Future studies should further quantify the benefits of nonsmoking, both for cancer prevention and for improving survival among CRC patients, in particular also in terms of treatment response.

  4. Müezzinler A, Mons U, Gellert C, Schöttker B, Jansen E, Kee F, et al.
    Am J Prev Med, 2015 Nov;49(5):e53-e63.
    PMID: 26188685 DOI: 10.1016/j.amepre.2015.04.004
    INTRODUCTION: Smoking is known to be a major cause of death among middle-aged adults, but evidence on its impact and the benefits of smoking cessation among older adults has remained limited. Therefore, we aimed to estimate the influence of smoking and smoking cessation on all-cause mortality in people aged ≥60 years.

    METHODS: Relative mortality and mortality rate advancement periods (RAPs) were estimated by Cox proportional hazards models for the population-based prospective cohort studies from Europe and the U.S. (CHANCES [Consortium on Health and Ageing: Network of Cohorts in Europe and the U.S.]), and subsequently pooled by individual participant meta-analysis. Statistical analyses were performed from June 2013 to March 2014.

    RESULTS: A total of 489,056 participants aged ≥60 years at baseline from 22 population-based cohort studies were included. Overall, 99,298 deaths were recorded. Current smokers had 2-fold and former smokers had 1.3-fold increased mortality compared with never smokers. These increases in mortality translated to RAPs of 6.4 (95% CI=4.8, 7.9) and 2.4 (95% CI=1.5, 3.4) years, respectively. A clear positive dose-response relationship was observed between number of currently smoked cigarettes and mortality. For former smokers, excess mortality and RAPs decreased with time since cessation, with RAPs of 3.9 (95% CI=3.0, 4.7), 2.7 (95% CI=1.8, 3.6), and 0.7 (95% CI=0.2, 1.1) for those who had quit <10, 10 to 19, and ≥20 years ago, respectively.

    CONCLUSIONS: Smoking remains as a strong risk factor for premature mortality in older individuals and cessation remains beneficial even at advanced ages. Efforts to support smoking abstinence at all ages should be a public health priority.

  5. Scelo G, Muller DC, Riboli E, Johansson M, Cross AJ, Vineis P, et al.
    Clin Cancer Res, 2018 Nov 15;24(22):5594-5601.
    PMID: 30037816 DOI: 10.1158/1078-0432.CCR-18-1496
    Purpose: Renal cell carcinoma (RCC) has the potential for cure with surgery when diagnosed at an early stage. Kidney injury molecule-1 (KIM-1) has been shown to be elevated in the plasma of RCC patients. We aimed to test whether plasma KIM-1 could represent a means of detecting RCC prior to clinical diagnosis.Experimental Design: KIM-1 concentrations were measured in prediagnostic plasma from 190 RCC cases and 190 controls nested within a population-based prospective cohort study. Cases had entered the cohort up to 5 years before diagnosis, and controls were matched on cases for date of birth, date at blood donation, sex, and country. We applied conditional logistic regression and flexible parametric survival models to evaluate the association between plasma KIM-1 concentrations and RCC risk and survival.Results: The incidence rate ratio (IRR) of RCC for a doubling in KIM-1 concentration was 1.71 [95% confidence interval (CI), 1.44-2.03, P = 4.1 × 10-23], corresponding to an IRR of 63.3 (95% CI, 16.2-246.9) comparing the 80th to the 20th percentiles of the KIM-1 distribution in this sample. Compared with a risk model including known risk factors of RCC (age, sex, country, body mass index, and tobacco smoking status), a risk model additionally including KIM-1 substantially improved discrimination between cases and controls (area under the receiver-operating characteristic curve of 0.8 compared with 0.7). High plasma KIM-1 concentrations were also associated with poorer survival (P = 0.0053).Conclusions: Plasma KIM-1 concentrations could predict RCC incidence up to 5 years prior to diagnosis and were associated with poorer survival. Clin Cancer Res; 24(22); 5594-601. ©2018 AACR.
  6. Lu Y, Beeghly-Fadiel A, Wu L, Guo X, Li B, Schildkraut JM, et al.
    Cancer Res, 2018 Sep 15;78(18):5419-5430.
    PMID: 30054336 DOI: 10.1158/0008-5472.CAN-18-0951
    Large-scale genome-wide association studies (GWAS) have identified approximately 35 loci associated with epithelial ovarian cancer (EOC) risk. The majority of GWAS-identified disease susceptibility variants are located in noncoding regions, and causal genes underlying these associations remain largely unknown. Here, we performed a transcriptome-wide association study to search for novel genetic loci and plausible causal genes at known GWAS loci. We used RNA sequencing data (68 normal ovarian tissue samples from 68 individuals and 6,124 cross-tissue samples from 369 individuals) and high-density genotyping data from European descendants of the Genotype-Tissue Expression (GTEx V6) project to build ovarian and cross-tissue models of genetically regulated expression using elastic net methods. We evaluated 17,121 genes for their cis-predicted gene expression in relation to EOC risk using summary statistics data from GWAS of 97,898 women, including 29,396 EOC cases. With a Bonferroni-corrected significance level of P < 2.2 × 10-6, we identified 35 genes, including FZD4 at 11q14.2 (Z = 5.08, P = 3.83 × 10-7, the cross-tissue model; 1 Mb away from any GWAS-identified EOC risk variant), a potential novel locus for EOC risk. All other 34 significantly associated genes were located within 1 Mb of known GWAS-identified loci, including 23 genes at 6 loci not previously linked to EOC risk. Upon conditioning on nearby known EOC GWAS-identified variants, the associations for 31 genes disappeared and three genes remained (P < 1.47 × 10-3). These data identify one novel locus (FZD4) and 34 genes at 13 known EOC risk loci associated with EOC risk, providing new insights into EOC carcinogenesis.Significance: Transcriptomic analysis of a large cohort confirms earlier GWAS loci and reveals FZD4 as a novel locus associated with EOC risk. Cancer Res; 78(18); 5419-30. ©2018 AACR.
  7. Phelan CM, Kuchenbaecker KB, Tyrer JP, Kar SP, Lawrenson K, Winham SJ, et al.
    Nat Genet, 2017 May;49(5):680-691.
    PMID: 28346442 DOI: 10.1038/ng.3826
    To identify common alleles associated with different histotypes of epithelial ovarian cancer (EOC), we pooled data from multiple genome-wide genotyping projects totaling 25,509 EOC cases and 40,941 controls. We identified nine new susceptibility loci for different EOC histotypes: six for serous EOC histotypes (3q28, 4q32.3, 8q21.11, 10q24.33, 18q11.2 and 22q12.1), two for mucinous EOC (3q22.3 and 9q31.1) and one for endometrioid EOC (5q12.3). We then performed meta-analysis on the results for high-grade serous ovarian cancer with the results from analysis of 31,448 BRCA1 and BRCA2 mutation carriers, including 3,887 mutation carriers with EOC. This identified three additional susceptibility loci at 2q13, 8q24.1 and 12q24.31. Integrated analyses of genes and regulatory biofeatures at each locus predicted candidate susceptibility genes, including OBFC1, a new candidate susceptibility gene for low-grade and borderline serous EOC.
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