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2.
  • Coignard, J, et al. (author)
  • A case-only study to identify genetic modifiers of breast cancer risk for BRCA1/BRCA2 mutation carriers
  • 2021
  • In: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 12:1, s. 1078-
  • Journal article (peer-reviewed)abstract
    • Breast cancer (BC) risk for BRCA1 and BRCA2 mutation carriers varies by genetic and familial factors. About 50 common variants have been shown to modify BC risk for mutation carriers. All but three, were identified in general population studies. Other mutation carrier-specific susceptibility variants may exist but studies of mutation carriers have so far been underpowered. We conduct a novel case-only genome-wide association study comparing genotype frequencies between 60,212 general population BC cases and 13,007 cases with BRCA1 or BRCA2 mutations. We identify robust novel associations for 2 variants with BC for BRCA1 and 3 for BRCA2 mutation carriers, P < 10−8, at 5 loci, which are not associated with risk in the general population. They include rs60882887 at 11p11.2 where MADD, SP11 and EIF1, genes previously implicated in BC biology, are predicted as potential targets. These findings will contribute towards customising BC polygenic risk scores for BRCA1 and BRCA2 mutation carriers.
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  • Dareng, EO, et al. (author)
  • Polygenic risk modeling for prediction of epithelial ovarian cancer risk
  • 2022
  • In: European journal of human genetics : EJHG. - : Springer Science and Business Media LLC. - 1476-5438 .- 1018-4813. ; 30:3, s. 349-362
  • Journal article (peer-reviewed)abstract
    • Polygenic risk scores (PRS) for epithelial ovarian cancer (EOC) have the potential to improve risk stratification. Joint estimation of Single Nucleotide Polymorphism (SNP) effects in models could improve predictive performance over standard approaches of PRS construction. Here, we implemented computationally efficient, penalized, logistic regression models (lasso, elastic net, stepwise) to individual level genotype data and a Bayesian framework with continuous shrinkage, “select and shrink for summary statistics” (S4), to summary level data for epithelial non-mucinous ovarian cancer risk prediction. We developed the models in a dataset consisting of 23,564 non-mucinous EOC cases and 40,138 controls participating in the Ovarian Cancer Association Consortium (OCAC) and validated the best models in three populations of different ancestries: prospective data from 198,101 women of European ancestries; 7,669 women of East Asian ancestries; 1,072 women of African ancestries, and in 18,915 BRCA1 and 12,337 BRCA2 pathogenic variant carriers of European ancestries. In the external validation data, the model with the strongest association for non-mucinous EOC risk derived from the OCAC model development data was the S4 model (27,240 SNPs) with odds ratios (OR) of 1.38 (95% CI: 1.28–1.48, AUC: 0.588) per unit standard deviation, in women of European ancestries; 1.14 (95% CI: 1.08–1.19, AUC: 0.538) in women of East Asian ancestries; 1.38 (95% CI: 1.21–1.58, AUC: 0.593) in women of African ancestries; hazard ratios of 1.36 (95% CI: 1.29–1.43, AUC: 0.592) in BRCA1 pathogenic variant carriers and 1.49 (95% CI: 1.35–1.64, AUC: 0.624) in BRCA2 pathogenic variant carriers. Incorporation of the S4 PRS in risk prediction models for ovarian cancer may have clinical utility in ovarian cancer prevention programs.
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  • Dennis, J, et al. (author)
  • Rare germline copy number variants (CNVs) and breast cancer risk
  • 2022
  • In: Communications biology. - : Springer Science and Business Media LLC. - 2399-3642. ; 5:1, s. 65-
  • Journal article (peer-reviewed)abstract
    • Germline copy number variants (CNVs) are pervasive in the human genome but potential disease associations with rare CNVs have not been comprehensively assessed in large datasets. We analysed rare CNVs in genes and non-coding regions for 86,788 breast cancer cases and 76,122 controls of European ancestry with genome-wide array data. Gene burden tests detected the strongest association for deletions in BRCA1 (P = 3.7E−18). Nine other genes were associated with a p-value < 0.01 including known susceptibility genes CHEK2 (P = 0.0008), ATM (P = 0.002) and BRCA2 (P = 0.008). Outside the known genes we detected associations with p-values < 0.001 for either overall or subtype-specific breast cancer at nine deletion regions and four duplication regions. Three of the deletion regions were in established common susceptibility loci. To the best of our knowledge, this is the first genome-wide analysis of rare CNVs in a large breast cancer case-control dataset. We detected associations with exonic deletions in established breast cancer susceptibility genes. We also detected suggestive associations with non-coding CNVs in known and novel loci with large effects sizes. Larger sample sizes will be required to reach robust levels of statistical significance.
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5.
  • Dork, T, et al. (author)
  • Two truncating variants in FANCC and breast cancer risk
  • 2019
  • In: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 9:1, s. 12524-
  • Journal article (peer-reviewed)abstract
    • Fanconi anemia (FA) is a genetically heterogeneous disorder with 22 disease-causing genes reported to date. In some FA genes, monoallelic mutations have been found to be associated with breast cancer risk, while the risk associations of others remain unknown. The gene for FA type C, FANCC, has been proposed as a breast cancer susceptibility gene based on epidemiological and sequencing studies. We used the Oncoarray project to genotype two truncating FANCC variants (p.R185X and p.R548X) in 64,760 breast cancer cases and 49,793 controls of European descent. FANCC mutations were observed in 25 cases (14 with p.R185X, 11 with p.R548X) and 26 controls (18 with p.R185X, 8 with p.R548X). There was no evidence of an association with the risk of breast cancer, neither overall (odds ratio 0.77, 95%CI 0.44–1.33, p = 0.4) nor by histology, hormone receptor status, age or family history. We conclude that the breast cancer risk association of these two FANCC variants, if any, is much smaller than for BRCA1, BRCA2 or PALB2 mutations. If this applies to all truncating variants in FANCC it would suggest there are differences between FA genes in their roles on breast cancer risk and demonstrates the merit of large consortia for clarifying risk associations of rare variants.
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6.
  • Escala-Garcia, M, et al. (author)
  • Germline variants and breast cancer survival in patients with distant metastases at primary breast cancer diagnosis
  • 2021
  • In: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 11:1, s. 19787-
  • Journal article (peer-reviewed)abstract
    • Breast cancer metastasis accounts for most of the deaths from breast cancer. Identification of germline variants associated with survival in aggressive types of breast cancer may inform understanding of breast cancer progression and assist treatment. In this analysis, we studied the associations between germline variants and breast cancer survival for patients with distant metastases at primary breast cancer diagnosis. We used data from the Breast Cancer Association Consortium (BCAC) including 1062 women of European ancestry with metastatic breast cancer, 606 of whom died of breast cancer. We identified two germline variants on chromosome 1, rs138569520 and rs146023652, significantly associated with breast cancer-specific survival (P = 3.19 × 10−8 and 4.42 × 10−8). In silico analysis suggested a potential regulatory effect of the variants on the nearby target genes SDE2 and H3F3A. However, the variants showed no evidence of association in a smaller replication dataset. The validation dataset was obtained from the SNPs to Risk of Metastasis (StoRM) study and included 293 patients with metastatic primary breast cancer at diagnosis. Ultimately, larger replication studies are needed to confirm the identified associations.
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  • Larsson, Susanna C, et al. (author)
  • Association of diet with serum insulin-like growth factor I in middle-aged and elderly men
  • 2005
  • In: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 81:5, s. 1163-7
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Insulin-like growth factor I (IGF-I) has been implicated in several chronic diseases, including cancer, heart disease, and osteoporosis.OBJECTIVE: Our aim was to assess whether intakes of total energy, alcohol, vitamins, minerals, and foods rich in protein and minerals (including red meat, fish and seafood, poultry, and milk) are associated with serum IGF-I concentrations in middle-aged and elderly men.DESIGN: We measured serum IGF-I concentrations in 226 free-living healthy men aged 42-76 y. The average of fourteen 24-h dietary telephone interviews performed over 1 y was used to estimate long-term dietary intake.RESULTS: We observed statistically significant positive associations between intakes of protein (P for trend = 0.001) and zinc (P for trend = 0.002) and serum IGF-I concentrations after adjusting for age. The difference in mean IGF-I concentrations for the highest compared with the lowest quintile of intake was approximately 17% (162 microg/L compared with 139 microg/L) for protein and approximately 16% (166 microg/L compared with 143 microg/L) for zinc. Consumption of red meat (P for trend = 0.05) and fish and seafood (P for trend = 0.07) was modestly positively associated with IGF-I concentrations. Other dietary factors were not associated with IGF-I concentrations.CONCLUSION: In this population of healthy well-nourished men, greater dietary intakes of protein, zinc, red meat, and fish and seafood were associated with higher IGF-I concentrations.
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9.
  • Liu, JJ, et al. (author)
  • Germline HOXB13 mutations p.G84E and p.R217C do not confer an increased breast cancer risk
  • 2020
  • In: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 10:1, s. 9688-
  • Journal article (peer-reviewed)abstract
    • In breast cancer, high levels of homeobox protein Hox-B13 (HOXB13) have been associated with disease progression of ER-positive breast cancer patients and resistance to tamoxifen treatment. Since HOXB13 p.G84E is a prostate cancer risk allele, we evaluated the association between HOXB13 germline mutations and breast cancer risk in a previous study consisting of 3,270 familial non-BRCA1/2 breast cancer cases and 2,327 controls from the Netherlands. Although both recurrent HOXB13 mutations p.G84E and p.R217C were not associated with breast cancer risk, the risk estimation for p.R217C was not very precise. To provide more conclusive evidence regarding the role of HOXB13 in breast cancer susceptibility, we here evaluated the association between HOXB13 mutations and increased breast cancer risk within 81 studies of the international Breast Cancer Association Consortium containing 68,521 invasive breast cancer patients and 54,865 controls. Both HOXB13 p.G84E and p.R217C did not associate with the development of breast cancer in European women, neither in the overall analysis (OR = 1.035, 95% CI = 0.859–1.246, P = 0.718 and OR = 0.798, 95% CI = 0.482–1.322, P = 0.381 respectively), nor in specific high-risk subgroups or breast cancer subtypes. Thus, although involved in breast cancer progression, HOXB13 is not a material breast cancer susceptibility gene.
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  • O'Mara, TA, et al. (author)
  • Identification of nine new susceptibility loci for endometrial cancer
  • 2018
  • In: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 9:1, s. 3166-
  • Journal article (peer-reviewed)abstract
    • Endometrial cancer is the most commonly diagnosed cancer of the female reproductive tract in developed countries. Through genome-wide association studies (GWAS), we have previously identified eight risk loci for endometrial cancer. Here, we present an expanded meta-analysis of 12,906 endometrial cancer cases and 108,979 controls (including new genotype data for 5624 cases) and identify nine novel genome-wide significant loci, including a locus on 12q24.12 previously identified by meta-GWAS of endometrial and colorectal cancer. At five loci, expression quantitative trait locus (eQTL) analyses identify candidate causal genes; risk alleles at two of these loci associate with decreased expression of genes, which encode negative regulators of oncogenic signal transduction proteins (SH2B3 (12q24.12) and NF1 (17q11.2)). In summary, this study has doubled the number of known endometrial cancer risk loci and revealed candidate causal genes for future study.
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  • Adami, Hans-Olov, et al. (author)
  • The aetiology and pathogenesis of human breast cancer
  • 1995
  • In: Mutation research. - 0027-5107 .- 1873-135X. ; 333:1-2, s. 29-35
  • Journal article (peer-reviewed)abstract
    • Whilst investigators have clearly shown that non-hereditary factors dominate the aetiology of human breast cancer, they have failed to identify quantitatively important causes, and prospects for prevention remain indeed limited. However, progress in epidemiological and basic research has taken place during the last few years. Current evidence suggests that breast cancer may be affected by the intra-uterine environment, that exposures during adolescence are particularly important, and that pregnancy has a dual effect on breast cancer risk: an early increase followed by long-term protection. Great variation exists in the structural development of the breast ductal system already in the newborn--and by inference in utero--and a pregnancy induces permanent structural changes in the mammary gland. We suggest that these observations fit into an aetiological model with the following key components: (1) breast cancer risk depends on the number of cells at risk, the susceptibility of individual cells to malignant transformation, and on the degree of cellular proliferation, notably cells which can act as founders of breast cancer; (2) the number of target cells is determined by the hormonal environment mainly early in life, perhaps already in utero; (3) in adult life, hormones which are non-genotoxic, increase breast cancer risk by increasing selective cell proliferation and thus number of target cells and the risk of retention of spontaneous somatic mutations; (4) while a pregnancy stimulates the growth of already malignant cells or cells close to malignant transformation (and thereby entails a short-term risk increase) the dominating long-term protection occurs due to permanent structural changes, terminal differentiation and perhaps decreased cell proliferation and carcinogen-binding in combination.
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  • Adams, Charleen, et al. (author)
  • Circulating Metabolic Biomarkers of Screen-Detected Prostate Cancer in the ProtecT Study
  • 2019
  • In: Cancer Epidemiology, Biomarkers and Prevention. - : American Association for Cancer Research (AACR). - 1055-9965 .- 1538-7755. ; 28:1, s. 208-216
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Whether associations between circulating metabolites and prostate cancer are causal is unknown. We report on the largest study of metabolites and prostate cancer (2,291 cases and 2,661 controls) and appraise causality for a subset of the prostate cancer-metabolite associations using two-sample Mendelian randomization (MR).MATERIALS AND METHODS: The case-control portion of the study was conducted in nine UK centres with men aged 50-69 years who underwent prostate-specific antigen (PSA) screening for prostate cancer within the Prostate testing for cancer and Treatment (ProtecT) trial. Two data sources were used to appraise causality: a genome-wide association study (GWAS) of metabolites in 24,925 participants and a GWAS of prostate cancer in 44,825 cases and 27,904 controls within the Association Group to Investigate Cancer Associated Alterations in the Genome (PRACTICAL) consortium.RESULTS: Thirty-five metabolites were strongly associated with prostate cancer (p <0.0014, multiple-testing threshold). These fell into four classes: i) lipids and lipoprotein subclass characteristics (total cholesterol and ratios, cholesterol esters and ratios, free cholesterol and ratios, phospholipids and ratios, and triglyceride ratios); ii) fatty acids and ratios; iii) amino acids; iv) and fluid balance. Fourteen top metabolites were proxied by genetic variables, but MR indicated these were not causal.CONCLUSIONS: We identified 35 circulating metabolites associated with prostate cancer presence, but found no evidence of causality for those 14 testable with MR. Thus, the 14 MR-tested metabolites are unlikely to be mechanistically important in prostate cancer risk.IMPACT: The metabolome provides a promising set of biomarkers that may aid prostate cancer classification.
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  • Aglago, Elom K., et al. (author)
  • A Genetic Locus within the FMN1/GREM1 Gene Region Interacts with Body Mass Index in Colorectal Cancer Risk
  • 2023
  • In: Cancer Research. - : American Association For Cancer Research (AACR). - 0008-5472 .- 1538-7445. ; 83:15, s. 2572-2583
  • Journal article (peer-reviewed)abstract
    • Colorectal cancer risk can be impacted by genetic, environmental, and lifestyle factors, including diet and obesity. Gene-environment interactions (G × E) can provide biological insights into the effects of obesity on colorectal cancer risk. Here, we assessed potential genome-wide G × E interactions between body mass index (BMI) and common SNPs for colorectal cancer risk using data from 36,415 colorectal cancer cases and 48,451 controls from three international colorectal cancer consortia (CCFR, CORECT, and GECCO). The G × E tests included the conventional logistic regression using multiplicative terms (one degree of freedom, 1DF test), the two-step EDGE method, and the joint 3DF test, each of which is powerful for detecting G × E interactions under specific conditions. BMI was associated with higher colorectal cancer risk. The two-step approach revealed a statistically significant G×BMI interaction located within the Formin 1/Gremlin 1 (FMN1/GREM1) gene region (rs58349661). This SNP was also identified by the 3DF test, with a suggestive statistical significance in the 1DF test. Among participants with the CC genotype of rs58349661, overweight and obesity categories were associated with higher colorectal cancer risk, whereas null associations were observed across BMI categories in those with the TT genotype. Using data from three large international consortia, this study discovered a locus in the FMN1/GREM1 gene region that interacts with BMI on the association with colorectal cancer risk. Further studies should examine the potential mechanisms through which this locus modifies the etiologic link between obesity and colorectal cancer.SIGNIFICANCE: This gene-environment interaction analysis revealed a genetic locus in FMN1/GREM1 that interacts with body mass index in colorectal cancer risk, suggesting potential implications for precision prevention strategies.
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  • Ahearn, Thomas U., et al. (author)
  • Common variants in breast cancer risk loci predispose to distinct tumor subtypes
  • 2022
  • In: Breast Cancer Research. - : Springer Nature. - 1465-5411 .- 1465-542X. ; 24:1
  • Journal article (peer-reviewed)abstract
    • BackgroundGenome-wide association studies (GWAS) have identified multiple common breast cancer susceptibility variants. Many of these variants have differential associations by estrogen receptor (ER) status, but how these variants relate with other tumor features and intrinsic molecular subtypes is unclear.MethodsAmong 106,571 invasive breast cancer cases and 95,762 controls of European ancestry with data on 173 breast cancer variants identified in previous GWAS, we used novel two-stage polytomous logistic regression models to evaluate variants in relation to multiple tumor features (ER, progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2) and grade) adjusting for each other, and to intrinsic-like subtypes.ResultsEighty-five of 173 variants were associated with at least one tumor feature (false discovery rate < 5%), most commonly ER and grade, followed by PR and HER2. Models for intrinsic-like subtypes found nearly all of these variants (83 of 85) associated at p < 0.05 with risk for at least one luminal-like subtype, and approximately half (41 of 85) of the variants were associated with risk of at least one non-luminal subtype, including 32 variants associated with triple-negative (TN) disease. Ten variants were associated with risk of all subtypes in different magnitude. Five variants were associated with risk of luminal A-like and TN subtypes in opposite directions.ConclusionThis report demonstrates a high level of complexity in the etiology heterogeneity of breast cancer susceptibility variants and can inform investigations of subtype-specific risk prediction.
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  • Ahmed, Hanna N., et al. (author)
  • Coffee consumption and risk of heart failure in men : An analysis from the Cohort of Swedish Men
  • 2009
  • In: American Heart Journal. - : MOSBY-ELSEVIER. - 0002-8703 .- 1097-6744. ; 158:4, s. 667-672
  • Journal article (peer-reviewed)abstract
    • Background A previous study found that consuming 5 or more cups of coffee per day was associated with increased incidence of heart failure (HF). We sought to evaluate this association in a larger population. Methods We measured coffee consumption using food frequency questionnaires among 37,315 men without history of myocardial infarction, diabetes, or HE They were observed for HF hospitalization or mortality from January 1, 1998, until December 3 1, 2006, using record linkage to the Swedish inpatient and cause of death registries. Cox proportional hazards models adjusted for age, dietary, and demographic factors were used to calculate incidence rate ratios (RR) and 95% confidence intervals (CIs). Results For 9 years of follow-up, 784 men experienced an HF event. Compared to men who drank! l cup of coffee per day (unadjusted rate 29.9 HF events/ 10,000 person-years), RR were 0.87 (95% CI 0.69-1.11, unadjusted rate 29.2/10,000 person-years) for 2 cups/d, 0.89 (95% CI 0.70-1.14, unadjusted rate 25.1/10,000 person-years) for 3 cups/d, 0.89 (95% CI 0.69-1.15, unadjusted rate 25.0/10,000 person-years) for 4 cups/d, and 0.89 (95% CI 0.69-1.15, unadjusted rate 18.1/10,000 person-years) for >= 5 cups/d (P for trend in RR = .61). Conclusions This study did not support the hypothesis that high coffee consumption is associated with increased rates of HF hospitalization or mortality. (Am Heart J 2009;158:667-72.)
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  • Akesson, Agneta, et al. (author)
  • Combined effect of low-risk dietary and lifestyle behaviors in primary prevention of myocardial infarction in women
  • 2007
  • In: Archives of Internal Medicine. - Karolinska Inst, Inst Environm Med, Div Nutr Epidemiol, S-17177 Stockholm, Sweden. Boston Univ, Sch Med, Dept Pediat, Boston, MA 02118 USA. : AMER MEDICAL ASSOC. - 0003-9926 .- 1538-3679. ; 167:19, s. 2122-2127
  • Journal article (peer-reviewed)abstract
    • Background: Limited data are available on the benefit of combining healthy dietary and lifestyle behaviors in the prevention of myocardial infarction (MI) in women. Methods: We used factor analysis to identify a lowrisk behavior - based dietary pattern in 24 444 postmenopausal women from the population- based prospective Swedish Mammography Cohort who were free of diagnosed cancer, cardiovascular disease, and diabetes mellitus at baseline (September 15, 1997). We also defined 3 low- risk lifestyle factors: nonsmoking, waist- hip ratio less than the 75th percentile (< 0.85), and being physically active (at least 40 minutes of daily walking or bicycling and 1 hour of weekly exercise). Results: During 6.2 years (151 434 person- years) of followup, we ascertained 308 cases of primary MI. Two major identified dietary patterns, "healthy" and "alcohol," were significantly associated with decreased risk of MI. The low- risk diet (high scores for the healthy dietary pattern) characterized by a high intake of vegetables, fruit, whole grains, fish, and legumes, in combination with moderate alcohol consumption (>= 5 g of alcohol per day), along with the 3 low-risk lifestyle behaviors, was associated with 92% decreased risk (95% confidence interval, 72%- 98%) compared with findings in women without any low-risk diet and lifestyle factors. This combination of healthy behaviors, present in 5%, may prevent 77% of MIs in the study population. Conclusion: Most MIs in women may be preventable by consuming a healthy diet and moderate amounts of alcohol, being physically active, not smoking, and maintaining a healthy weight.
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  • Akesson, Agneta, et al. (author)
  • Dietary exposure to polychlorinated biphenyls and risk of heart failure - A population-based prospective cohort study
  • 2019
  • In: Environment International. - : PERGAMON-ELSEVIER SCIENCE LTD. - 0160-4120 .- 1873-6750. ; 126, s. 1-6
  • Journal article (peer-reviewed)abstract
    • Background: Beneficial effects of fish consumption on heart failure (HF) may be modified by contaminants in fish. Polychlorinated biphenyls (PCBs) are of particular concern as they have been associated with well-established risk factors of HF, but current data are limited. Objectives: We aimed to assess the association between dietary PCB exposure and risk of HF, accounting for dietary intake of long-chain omega-3 fish fatty acids. Design: We used the prospective population-based research structure SIMPLER (previously the Swedish Mammography Cohort and Cohort of Swedish Men) comprising 32,952 women and 36,546 men, free from cancer, cardiovascular disease and diabetes at baseline in 1997. Validated estimates of dietary PCBs and long-chain omega-3 fish fatty acids [eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA)] were obtained via a food frequency questionnaire at baseline. Incident cases of HF were ascertained through register linkage. Results: During an average of 12 years of follow-up, we ascertained 2736 and 3128 incident cases of HF in women and men, respectively. In multivariable-adjusted models, mutually adjusted for PCBs and EPA-DHA, the relative risk (RR) for dietary PCB exposure was 1.48 (95% CI 1.12-1.96) in women and 1.42 (95% CI 1.08-1.86) in men, comparing extreme quintiles. Corresponding RRs for EPA-DHA intake were 0.71 (95% CI 0.54-0.93) and 0.82 (95% CI 0.63-1.07), respectively. Conclusions: Dietary exposure to PCBs was associated with an increased risk of HF in both women and men. EPA-DHA intake was associated with a lower risk of HF in women, with a similar tendency in men.
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  • Akesson, Agneta, et al. (author)
  • Long-term dietary cadmium intake and postmenopausal endometrial cancer incidence : A population-based prospective cohort study
  • 2008
  • In: Cancer Research. - : AMER ASSOC CANCER RESEARCH. - 0008-5472 .- 1538-7445. ; 68:15, s. 6435-6441
  • Journal article (peer-reviewed)abstract
    • Environmental pollutants mimicking the effects of estrogen are suggested to contribute to the high incidence of hormone-related cancers, but supporting data are sparse. A potent estrogen-like activity of the pollutant cadmium, mediated via the estrogen receptor-alpha, has been shown in vivo. We prospectively examined the association between cadmium exposure and incidence of postmenopausal endometrial cancer. The Swedish Mammography Cohort is a population-based prospective cohort of 30,210 postmenopausal women free of cancer diagnose at baseline (1987) and who completed a food frequency questionnaire at baseline and in 1997. We estimated the dietary cadmium intake based on the questionnaire data and the cadmium content in all foods. During 16.0 years (484,274 person-years) of follow-up between the baseline and mid-2006, we ascertained 378 incident cases of endometrioid adenocarcinoma. The average estimated dietary cadmium intake was 15 mu g/day (80% from cereals and vegetables). Cadmium intake was statistically significantly associated with increased risk of endometrial cancer in all women; the multivariate relative risk (1111) was 1.39 [95% confidence interval (CI), 1.04-1.86; P-trend = 0.019], comparing highest tertile versus lowest. Among never-smoking women with body mass index (BMI) of <27 kg/m(2), the RR was 1.86 (95% CI, 1.13-3.08; P-trend = 0.009). We observed a 2.9-fold increased risk (95% CI, 1.05-7.79) associated with long-term cadmium intake consistently above the median at both baseline 1987 and in 1997 in never-smoking women with low bioavailable estrogen (BMI of <27 kg/m(2) and nonusers of postmenopausal hormones). Our results support the hypothesis that cadmium may exert estrogenic effects and thereby increase the risk of hormone-related cancers.
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  • Akesson, Agneta, et al. (author)
  • Low-Risk Diet and Lifestyle Habits in the Primary Prevention of Myocardial Infarction in Men A Population-Based Prospective Cohort Study
  • 2014
  • In: Journal of the American College of Cardiology. - : ELSEVIER SCIENCE INC. - 0735-1097 .- 1558-3597. ; 64:13, s. 1299-1306
  • Journal article (peer-reviewed)abstract
    • BACKGROUND Adherence to a combination of healthy dietary and lifestyle practices may have an impressive impact on the primary prevention of myocardial infarction (MI). OBJECTIVES The aim of this study was to examine the benefit of combined low-risk diet and healthy lifestyle practices on the incidence of MI in men. METHODS The population-based, prospective cohort of Swedish men comprised 45-to 79-year-old men who completed a detailed questionnaire on diet and lifestyle at baseline in 1997. In total, 20,721 men with no history of cancer, cardiovascular disease, diabetes, hypertension, or high cholesterol levels were followed through 2009. Low-risk behavior included 5 factors: a healthy diet (top quintile of Recommended Food Score), moderate alcohol consumption (10 to 30 g/day), no smoking, being physically active (walking/bicycling >= 40 min/day and exercising >= 1 h/week), and having no abdominal adiposity (waist circumference <95 cm). RESULTS During 11 years of follow-up, we ascertained 1,361 incident cases of MI. The low-risk dietary choice together with moderate alcohol consumption was associated with a relative risk of 0.65 (95% confidence interval [CI]: 0.48 to 0.87) compared with men having 0 of 5 low-risk factors. Men having all 5 low-risk factors compared with those with 0 low-risk factors had a relative risk of 0.14 (95% CI: 0.04 to 0.43). This combination of healthy behaviors, present in 1% of the men, could prevent 79% (95% CI: 34% to 93%) of the MI events on the basis of the study population. CONCLUSIONS Almost 4 of 5 MIs in men may be preventable with a combined low-risk behavior. (C) 2014 by the American College of Cardiology Foundation.
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  • Ali, Imran, et al. (author)
  • Exposure to polychlorinated biphenyls and prostate cancer : population-based prospective cohort and experimental studies
  • 2016
  • In: Carcinogenesis. - : Oxford University Press. - 0143-3334 .- 1460-2180. ; 37:12, s. 1144-1151
  • Journal article (peer-reviewed)abstract
    • Polychlorinated biphenyls (PCBs) are highly persistent environmental pollutants and are undesirable components of our daily food. PCBs are classified as human carcinogens, but the evidence for prostate cancer is limited and available data are inconsistent. We explored the link between non-dioxin-like PCB and grade of prostate cancer in a prospective cohort as well as in cell experiments. A population-based cohort of 32496 Swedish men aged 45-79 years was followed prospectively through 1998-2011, to assess the association between validated estimates of dietary PCB exposure and incidence of prostate cancer by grade (2789 cases, whereof 1276 low grade, 756 intermediate grade, 450 high grade) and prostate cancer mortality (357 fatal cases). In addition, we investigated a non-dioxin-like PCB153-induced cell invasion and related markers in normal prostate stem cells (WPE-stem) and in three different prostate cancer cell lines (PC3, DU145 and 22RV1) at exposure levels relevant to humans. After multivariable-adjustment, dietary PCB exposure was positively associated with high-grade prostate cancer, relative risk (RR) 1.35 [95% confidence interval (CI): 1.03-1.76] and with fatal prostate cancer, RR 1.43 (95% CI: 1.05-1.95), comparing the highest tertile with the lowest. We observed no association with low or intermediate grade of prostate cancer. Cell invasion and related markers, including MMP9, MMP2, Slug and Snail, were significantly increased in human prostate cancer cells as well as in prostate stem cells after exposure to PCB153. Our findings both from the observational and experimental studies suggest a role of non-dioxin-like PCB153 in the development of high-grade and fatal prostate cancer.
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25.
  • Almgren, Malin, et al. (author)
  • Adenovirus-36 Is Associated with Obesity in Children and Adults in Sweden as Determined by Rapid ELISA
  • 2012
  • In: PLOS ONE. - : PUBLIC LIBRARY SCIENCE. - 1932-6203. ; 7:7
  • Journal article (peer-reviewed)abstract
    • Background: Experimental and natural human adenovirus-36 (Adv36) infection of multiple animal species results in obesity through increasing adipogenesis and lipid accumulation in adipocytes. Presence of Adv36 antibodies detected by serum neutralization assay has previously been associated with obesity in children and adults living in the USA, South Korea and Italy, whereas no association with adult obesity was detected in Belgium/the Netherlands nor among USA military personnel. Adv36 infection has also been shown to reduce blood lipid levels, increase glucose uptake by adipose tissue and skeletal muscle biopsies, and to associate with improved glycemic control in non-diabetic individuals. Principal Findings: Using a novel ELISA, 1946 clinically well-characterized individuals including 424 children and 1522 nondiabetic adults, and 89 anonymous blood donors, residing in central Sweden representing the population in Stockholm area, were studied for the presence of antibodies against Adv36 in serum. The prevalence of Adv36 positivity in lean individuals increased from similar to 7% in 1992-1998 to 15-20% in 2002-2009, which paralleled the increase in obesity prevalence. We found that Adv36-positive serology was associated with pediatric obesity and with severe obesity in females compared to lean and overweight/mildly obese individuals, with a 1.5 to 2-fold Adv36 positivity increase in cases. Moreover, Adv36 positivity was less common among females and males on antilipid pharmacological treatment or with high blood triglyceride level. Insulin sensitivity, measured as lower HOMA-IR, showed a higher point estimate in Adv36-positive obese females and males, although it was not statistically significant (p = 0.08). Conclusion: Using a novel ELISA we show that Adv36 infection is associated with pediatric obesity, severe obesity in adult females and lower risk of high blood lipid levels in non-diabetic Swedish individuals.
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26.
  • Amzal, Billy, et al. (author)
  • Population Toxicokinetic Modeling of Cadmium for Health Risk Assessment
  • 2009
  • In: Journal of Environmental Health Perspectives. - : US DEPT HEALTH HUMAN SCIENCES PUBLIC HEALTH SCIENCE. - 0091-6765 .- 1552-9924. ; 117:8, s. 1293-1301
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Cadmium is a widespread environmental pollutant that has been shown to exert toxic effects on kidney and bones in humans after long-term exposure. Urinary cadmium concentration is considered a good biomarker of accumulated cadmium in kidney, and diet is the main source of cadmium among nonsmokers. OBJECTIVE: Modeling the link between urinary cadmium and dietary cadmium intake is a key step in the risk assessment of long-term cadmium exposure. There is, however, little knowledge on how this link may vary, especially for susceptible population strata. METHODS: We used a large population-based study (the Swedish Mammography Cohort), with repeated dietary intake data covering a period of 20 years, to compare estimated dietary cadmium intake with urinary cadmium concentrations on an individual basis. A modified version of the Nordberg-Kjellstrom model and a one-compartment model were evaluated in terms of their predictions of urinary cadmium. We integrated the models and quantified the between-person variability of cadmium half-life in the population. Finally, sensitivity analyses and Monte Carlo simulations were performed to illustrate how the latter model could serve as a robust tool supporting the risk assessment of cadmium in humans. RESULTS: The one-compartment population model appeared to be an adequate modeling option to link cadmium intake to urinary cadmium and to describe the population variability. We estimated the cadmium half-life to be about 11.6 years, with about 25% population variability. CONCLUSIONS: Population toxicokinetic models can be robust and useful tools for risk assessment of chemicals, because they allow quantification and integration of population variability in toxicokinetics.
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27.
  • Archambault, Alexi N., et al. (author)
  • Cumulative Burden of Colorectal Cancer Associated Genetic Variants Is More Strongly Associated With Early-Onset vs Late-Onset Cancer
  • 2020
  • In: Gastroenterology. - : Elsevier BV. - 0016-5085 .- 1528-0012. ; 158:5, s. 1274-1286.e12
  • Journal article (peer-reviewed)abstract
    • BACKGROUND & AIMS: Early-onset colorectal cancer (CRC, in persons younger than 50 years old) is increasing in incidence; yet, in the absence of a family history of CRC, this population lacks harmonized recommendations for prevention. We aimed to determine whether a polygenic risk score (PRS) developed from 95 CRC-associated common genetic risk variants was associated with risk for early-onset CRC.METHODS: We studied risk for CRC associated with a weighted PRS in 12,197 participants younger than 50 years old vs 95,865 participants 50 years or older. PRS was calculated based on single nucleotide polymorphisms associated with CRC in a large-scale genome-wide association study as of January 2019. Participants were pooled from 3 large consortia that provided clinical and genotyping data: the Colon Cancer Family Registry, the Colorectal Transdisciplinary Study, and the Genetics and Epidemiology of Colorectal Cancer Consortium and were all of genetically defined European descent. Findings were replicated in an independent cohort of 72,573 participants.RESULTS: Overall associations with CRC per standard deviation of PRS were significant for early-onset cancer, and were stronger compared with late-onset cancer (P for interaction = .01); when we compared the highest PRS quartile with the lowest, risk increased 3.7-fold for early-onset CRC (95% CI 3.28-4.24) vs 2.9-fold for late-onset CRC (95% CI 2.80-3.04). This association was strongest for participants without a first-degree family history of CRC (P for interaction = 5.61 x 10(-5)). When we compared the highest with the lowest quartiles in this group, risk increased 4.3-fold for early-onset CRC (95% CI 3.61-5.01) vs 2.9-fold for late-onset CRC (95% CI 2.70-3.00). Sensitivity analyses were consistent with these findings.CONCLUSIONS: In an analysis of associations with CRC per standard deviation of PRS, we found the cumulative burden of CRC-associated common genetic variants to associate with early-onset cancer, and to be more strongly associated with early-onset than late-onset cancer, particularly in the absence of CRC family history. Analyses of PRS, along with environmental and lifestyle risk factors, might identify younger individuals who would benefit from preventive measures.
  •  
28.
  •  
29.
  • Balder, Helena F, et al. (author)
  • Common and country-specific dietary patterns in four European cohort studies
  • 2003
  • In: Journal of Nutrition. - : Elsevier BV. - 0022-3166 .- 1541-6100. ; 133:12, s. 4246-51
  • Journal article (peer-reviewed)abstract
    • The association between diet and cancer, predominantly investigated univariately, has often been inconsistent, possibly because of the large number of candidate risk factors and their high intercorrelations. Analysis of dietary patterns is expected to give more insight than analysis of single nutrients or foods. This study aimed to develop and apply a common methodological approach to determine dietary patterns in four cohort studies originating in Finland, the Netherlands, Sweden and Italy. Food items on each of the food frequency questionnaires were aggregated into 51 food groups, defined on the basis of their position in the diet pattern and possible relevance to cancer etiology. Exploratory factor analysis was used to analyze dietary patterns. Using a standardized approach, 3-5 stable dietary patterns were identified, explaining 20-29% of total variance in consumption of the food groups. Two dietary patterns, which explained most of the variance, were consistent across the studies. The first pattern was characterized by high consumption of (salad) vegetables, the second by high consumption of pork, processed meat and potatoes. In addition, a few specifically national food patterns were identified. Sensitivity analyses showed that the identified patterns were robust for number of factors extracted, distribution of input variables and energy adjustment. Our findings suggest that some important eating patterns are shared by the four populations under study, whereas other eating patterns are population specific.
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30.
  • Bao, Ying, et al. (author)
  • Folate Intake and Risk of Pancreatic Cancer : Pooled Analysis of Prospective Cohort Studies
  • 2011
  • In: Journal of the National Cancer Institute. - : OXFORD UNIV PRESS INC. - 0027-8874 .- 1460-2105. ; 103:24, s. 1840-1850
  • Research review (peer-reviewed)abstract
    • Background Epidemiological studies evaluating the association between folate intake and risk of pancreatic cancer have produced inconsistent results. The statistical power to examine this association has been limited in previous studies partly because of small sample size and limited range of folate intake in some studies. Methods We analyzed primary data from 14 prospective cohort studies that included 319 716 men and 542 948 women to assess the association between folate intake and risk of pancreatic cancer. Folate intake was assessed through a validated food-frequency questionnaire at baseline in each study. Study-specific relative risks (RRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models and then pooled using a random effects model. All statistical tests were two-sided. Results During 7-20 years of follow-up across studies, 2195 pancreatic cancers were identified. No association was observed between folate intake and risk of pancreatic cancer in men and women (highest vs lowest quintile: dietary folate intake, pooled multivariable RR = 1.06, 95% CI = 0.90 to 1.25, P-trend = .47; total folate intake [dietary folate and supplemental folic acid], pooled multivariable RR = 0.96, 95% CI = 0.80 to 1.16, P-trend = .90). No between-study heterogeneity was observed (for dietary folate, P-heterogeneity = .15; for total folate, P-heterogeneity = .22). Conclusion Folate intake was not associated with overall risk of pancreatic cancer in this large pooled analysis.
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31.
  • Basu, Samar, et al. (author)
  • Inflammatory F2-isoprostane, prostaglandin F2α, pentraxin 3 levels and breast cancer risk : The Swedish Mammography Cohort
  • 2016
  • In: Prostaglandins, Leukotrienes and Essential Fatty Acids. - : Elsevier BV. - 0952-3278 .- 1532-2823. ; 113, s. 28-32
  • Journal article (peer-reviewed)abstract
    • INTRODUCTION: Breast cancer is a common cancer among women. Identifying cellular participation of F2-isoprostane, prostaglandin F2α (PGF2α) and pentraxin 3 (PTX3) in cancer we evaluated whether their prediagnostic systemic levels that originate from different inflammatory pathways were associated with breast cancer risk.METHODS: Seventy-eight breast cancer cases diagnosed after blood collection and 797 controls from the Swedish Mammography Cohort were analysed for urinary F2-isoprostane, PGF2α and plasma PTX3 levels.RESULTS: None of the biomarkers investigated were significantly associated with breast cancer risk. However, there was the suggestion of an inverse association with PTX3 with multivariable adjusted ORs (95% CI) of 0.56 (95% CI=0.29-1.06) and 0.67 (95% CI=0.35-1.28) for the second and third tertiles, respectively (ptrend=0.20). No associations were observed between F2-isoprostane (OR=0.87; 95% CI=0.48-1.57; ptrend=0.67) and PGF2α metabolite (OR=1.03; 95% CI=0.56-1.88; ptrend=0.91) comparing the top to bottom tertiles.CONCLUSIONS: The systemic levels of F2-isoprostane, PGF2α and PTX3 witnessed in women who later developed breast cancer may not provide prognostic information regarding tumor development in spite of their known involvement in situ cellular context. These observations may indicate that other mechanisms exist in controlling cellular formation of F2-isoprostane, PGF2α and PTX3 and their systemic availability in breast cancer patients.
  •  
32.
  • Basu, Samar, et al. (author)
  • Is There any Role for Serum Cathepsin S, CRP levels on Prognostic Information in Breast Cancer? : The Swedish Mammography Cohort
  • 2015
  • In: Antioxidants and Redox Signaling. - : Mary Ann Liebert Inc. - 1523-0864 .- 1557-7716. ; 23:16, s. 1298-1302
  • Journal article (peer-reviewed)abstract
    • Breast cancer is the most common cancer among women, and both low-grade inflammation and cathepsins might have important roles in breast cancer. We questioned whether prediagnostic circulating levels of C-reactive protein (CRP), cathepsin B and cathepsin S were associated with breast cancer risk. Sixty-nine incident breast cancer cases diagnosed after blood collection and 719 controls from the Swedish Mammography Cohort were analysed for systemic CRP, cathepsin B and cathepsin S. Cathepsin S and inflammation (hsCRP) adjusted cathepsin S were inversely associated with breast cancer risk (cathepsin S: OR for top vs. bottom tertile = 0.46; 95% CI = 0.23-0.92; Ptrend = 0.02; hsCRP adjusted cathepsin S: OR of 0.44; 95% CI = 0.22-0.87; Ptrend = 0.02). hsCRP was significantly associated with increased breast cancer risk (OR for top vs. bottom tertile= 2.01; 95% CI = 1.02-3.95; Ptrend = 0.04). No significant association was observed between cathepsin B and breast cancer risk (OR for top vs. bottom tertile= 0.67; 95% CI = 0.32-1.40; Ptrend = 0.30). These observations lead to hypothesis that levels of cathepsin S and hsCRP observed in women who later developed breast cancer may provide prognostic information regarding tumor development and need to be evaluated in prospective studies.
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33.
  • Bellavia, Andrea, et al. (author)
  • Alcohol consumption and mortality : a dose-response analysis in terms of time
  • 2014
  • In: Annals of Epidemiology. - : ELSEVIER SCIENCE INC. - 1047-2797 .- 1873-2585. ; 24:4, s. 291-296
  • Journal article (peer-reviewed)abstract
    • Purpose: Low-to-moderate alcohol consumption is associated with decreased mortality. However, many aspects of this association are still debated. Our aim was to complement available information by conducting a dose-response analysis of the association between alcohol consumption and survival time. Methods: In a Swedish population-based cohort of 67,706 middle-aged and elderly men and women, frequency and amount of drinking were assessed through a self-administrated questionnaire. During 15 years of follow-up, 13,323 participants died. Differences in survival (10th percentile differences, PDs) according to levels of alcohol consumption were estimated using Laplace regression. Results: We found evidence of nonlinearity between alcohol consumption and survival. Among women, we observed a rapid increase in survival up to 6 g/d of alcohol consumption (0.5 drinks/d) where survival was 17 months longer (PD = 17 months, 95% confidence interval, 10 to 24). After this peak, higher alcohol consumption was progressively associated with shorter survival. Among men, survival improved up to 15 g/d (1.5 drinks/d) where we observed a PD of 15 months (95% confidence interval, 8 to 22). Conclusions: Low alcohol consumption was associated with improved survival up to 1.5 years for women with an average consumption of 0.5 drinks per day and to 13 years for men with an average consumption of 1.5 drinks per day. (C) 2014 Elsevier Inc. All rights reserved.
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34.
  • Bellavia, Andrea, et al. (author)
  • Differences in age at death according to smoking and age at menopause
  • 2016
  • In: Menopause. - : LIPPINCOTT WILLIAMS & WILKINS. - 1072-3714 .- 1530-0374. ; 23:1, s. 108-110
  • Journal article (peer-reviewed)abstract
    • Objective: Younger age at menopause is associated with overall mortality, and cigarette smoking is the only lifestyle factor influencing this association. However, the combined effects of age at menopause and smoking have never been quantified in terms of survival time. Our aim was to evaluate, in a large cohort of Swedish women, differences in age at death according to age at menopause and smoking status. Methods: Age at menopause and smoking were assessed, using a self-administered questionnaire, in a population-based cohort of 25,474 women aged 48 to 83 years. Laplace regression was used to calculate differences in median age at death (50th percentile difference [PD]) according to smoking and age at menopause. Results: Across 16 years of follow-up, 5,942 participants died. The difference in median age at death between women with menopause at 40 years and women with menopause at 60 years was 1.3 years (50th PD, 1.3; 95% CI, 0.3-2.2). Compared with current smokers, former smokers and never smokers had older median age at death-2.5 years (50th PD, 2.5; 95% CI, 1.9-3.1) and 3.6 years (50th PD, 3.6; 95% CI, 3.1-4.1), respectively. When analysis was restricted to current smokers, the difference in age at death between women with menopause at 40 years and women with menopause at 60 years increased to 2.6 years (50th PD, 2.6; 95% CI, 0.8-4.5). No association among never smokers was observed. Conclusions: Younger age at menopause is linearly associated with shorter survival. This association tends to be stronger among current smokers.
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35.
  • Bellavia, Andrea, et al. (author)
  • Differences in survival associated with processed and with nonprocessed red meat consumption
  • 2014
  • In: American Journal of Clinical Nutrition. - : OXFORD UNIV PRESS. - 0002-9165 .- 1938-3207. ; 100:3, s. 924-929
  • Journal article (peer-reviewed)abstract
    • Background: High red meat consumption is associated with an increased mortality risk. This association is partly explained by the negative effect of processed meat consumption, which is widely established. The role of nonprocessed meat is unclear. Objective: The objective was to examine the combined association of processed and nonprocessed meat consumption with survival in a Swedish large prospective cohort. Design: In a population-based cohort of 74,645 Swedish men (40,089) and women (34,556), red meat consumption was assessed through a self-administered questionnaire. We estimated differences in survival [15th percentile differences (PDs), differences in the time by which the first 15% of the cohort died] according to levels of total red meat and combined levels of processed and nonprocessed red meat consumption. Results: During 15 y of follow-up (January 1998 to December 2012), we documented 16,683 deaths (6948 women; 9735 men). Compared with no consumption, consumption of red meat >100 g/d was progressively associated with shorter survival-up to 2 y for participants consuming an average of 300 g/d (15th PD: -21 mo; 95% CI: -31, -10). Compared with no consumption, high consumption of processed red meat (100 g/d) was associated with shorter survival (15th PD: -9 mo; 95% CI: -16, -2). High and moderate intakes of nonprocessed red meat were associated with shorter survival only when accompanied by a high intake of processed red meat. Conclusions: We found that high total red meat consumption was associated with progressively shorter survival, largely because of the consumption of processed red meat. Consumption of nonprocessed red meat alone was not associated with shorter survival. The Swedish Mammography Cohort and the Cohort of Swedish Men were registered at clinicaltrials.gov as NCT01127698 and NCT01127711, respectively.
  •  
36.
  • Bellavia, A, et al. (author)
  • Fish consumption and all-cause mortality in a cohort of Swedish men and women.
  • 2017
  • In: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 281:1, s. 86-95
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Epidemiological studies of fish consumption and all-cause mortality have provided inconsistent results.OBJECTIVE: We examined the dose-response association between fish consumption and mortality from all causes in a large population-based cohort of Swedish men and women.METHODS: The study included 72 522 participants (33 973 women and 38 549 men), aged 45-83 years, from the Swedish Mammography Cohort and the Cohort of Swedish Men. Information on fish consumption was obtained through a self-administered questionnaire in 1997. Participants were followed for 17 years (1 January 1998 to 31 December 2014), and data on death and causes of death were ascertained through linkage to the Swedish Cause of Death Register. We used Cox proportional hazard regression to estimate hazard ratios (HRs) of death. Fish consumption was evaluated as a continuous predictor, flexibly modelled with restricted cubic splines to assess potential nonlinear associations.RESULTS: During follow-up, 16 730 deaths (7168 women and 9562 men) were recorded. The dose-response association between fish consumption and all-cause mortality was U-shaped. Compared with the median fish consumption (women: 25.0; men: 30.5 g day-1 ), lower levels of consumption were progressively associated with higher mortality risk up to 25% for women [HR 1.25; 95% confidence interval (CI): 1.11, 1.40] and 19% for men (HR 1.19; 95% CI: 1.07, 1.32) with no reported consumption. Increasingly higher levels of fish consumption were associated with higher mortality risk only amongst women, with a 39% higher mortality risk amongst women reporting the highest level of fish consumption (80 g day-1 ; HR 1.39; 95% CI: 1.15, 1.68).CONCLUSION: These results indicate a U-shaped association between fish consumption and all-cause mortality, particularly amongst women.
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37.
  • Bellavia, Andrea, et al. (author)
  • Fruit and vegetable consumption and all-cause mortality : a dose-response analysis.
  • 2013
  • In: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 98:2, s. 454-459
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: The association between fruit and vegetable (FV) consumption and overall mortality has seldom been investigated in large cohort studies. Findings from the few available studies are inconsistent.OBJECTIVE: The objective was to examine the dose-response relation between FV consumption and mortality, in terms of both time and rate, in a large prospective cohort of Swedish men and women.DESIGN: FV consumption was assessed through a self-administrated questionnaire in a population-based cohort of 71,706 participants (38,221 men and 33,485 women) aged 45-83 y. We performed a dose-response analysis to evaluate 10th survival percentile differences (PDs) by using Laplace regression and estimated HRs by using Cox regression.RESULTS: During 13 y of follow-up, 11,439 deaths (6803 men and 4636 women) occurred in the cohort. In comparison with 5 servings FV/d, a lower consumption was progressively associated with shorter survival and higher mortality rates. Those who never consumed FV lived 3 y shorter (PD: -37 mo; 95% CI: -58, -16 mo) and had a 53% higher mortality rate (HR: 1.53; 95% CI: 1.19, 1.99) than did those who consumed 5 servings FV/d. Consideration of fruit and vegetables separately showed that those who never consumed fruit lived 19 mo shorter (PD: -19 mo; 95% CI: -29, -10 mo) than did those who ate 1 fruit/d. Participants who consumed 3 vegetables/d lived 32 mo longer than did those who never consumed vegetables (PD: 32 mo; 96% CI: 13, 51 mo).CONCLUSION: FV consumption <5 servings/d is associated with progressively shorter survival and higher mortality rates. The Swedish Mammography Cohort and the Cohort of Swedish Men were registered at clinicaltrials.gov as NCT01127698 and NCT01127711, respectively.
  •  
38.
  • Bellavia, Andrea, et al. (author)
  • High red meat intake and all-cause cardiovascular and cancer mortality : is the risk modified by fruit and vegetable intake?
  • 2016
  • In: American Journal of Clinical Nutrition. - : OXFORD UNIV PRESS. - 0002-9165 .- 1938-3207. ; 104:4, s. 1137-1143
  • Journal article (peer-reviewed)abstract
    • Background: High red meat consumption is associated with a shorter survival and higher risk of cardiovascular disease (CVD), cancer, and all-cause mortality. Fruit and vegetable (FV) consumption is associated with a longer survival and lower mortality risk. Whether high FV consumption can counterbalance the negative impact of high red meat consumption is unknown. Objective: We evaluated 2 large prospective cohorts of Swedish men and women (the Swedish Mammography Cohort and the Cohort of Swedish Men) to determine whether the association between red meat consumption and the risk of all-cause, CVD, and cancer specific mortality differs across amounts of FV intake. Design: The study population included 74,645 Swedish men and women. Red meat and FV consumption were assessed through a self-administered questionnaire. We estimated HRs of all-cause, CVD, and cancer mortality according to quintiles of total red meat consumption. We next investigated possible interactions between red meat and FV consumption and evaluated the dose-response associations at low, medium, and high FV intake. Results: Compared with participants in the lowest quintile of total red meat consumption, those in the highest quintile had a 21% increased risk of all-cause mortality (HR: 1.21; 95% CI: 1.13, 1.29), a 29% increased risk of CVD mortality (BR: 1.29; 95% CI: 1.14, 1.46), and no increase in the risk of cancer mortality (HR: 1.00; 95% CI: 0.88, 1.43). Results were remarkably similar across amounts of FV consumption, and no interaction between red meat and FV consumption was detected. Conclusion: High intakes of red meat were associated with a higher risk of all-cause and CVD mortality. The increased risks were consistently observed in participants with low, medium, and high FV consumption. The Swedish Mammography Cohort and the Cohort of Swedish Men were registered at clinicaltrials.gov as NCT01127698 and NCT01127711, respectively.
  •  
39.
  • Bellavia, Andrea, et al. (author)
  • Physical activity and mortality in a prospective cohort of middle-aged and elderly men - : a time perspective.
  • 2013
  • In: International Journal of Behavioral Nutrition and Physical Activity. - : Springer Science and Business Media LLC. - 1479-5868. ; 10
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Higher physical activity (PA) levels are known to be associated with lower risk of death. Less attention, however, has been paid to directly evaluate the effect of PA on the time by which a certain fraction of the population has died.METHODS: A population-based cohort of 29,362 men 45 to 79 years of age was followed from January 1998 to December 2010. A total of 4,570 men died. PA was assessed through a self-administrated questionnaire. Adjusted differences in the number of months by which 10% (10th percentile) of the cohort has died, according to levels of total PA (TPA) and different domains of PA were estimated using Laplace regression.RESULTS: Overall, the 10th survival percentile was 9.6 years, that is, 90% of the cohort lived longer than 9.6 years. We found a strong evidence of non-linearity between TPA and the 10th survival percentile (P-value < 0.001). Compared to men with the lowest TPA (29 metabolic equivalents (MET)-hrs/day), men with a median TPA (41 MET-hrs/day) had 30 months longer survival (95% CI: 25-35). Below the median TPA, every increment of 4 MET-hrs/day, approximately a 30 minutes brisk pace daily walk, was associated with a longer survival of 11 months (95% CI: 8-15). Above the median TPA additional activity was not significantly associated with better survival.CONCLUSIONS: We found that a physically active lifestyle is associated with a substantial improvement in survival time, up to 2.5 years over 13 years of follow-up.
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40.
  • Bellavia, Andrea, et al. (author)
  • Quantifying the benefits of Mediterranean diet in terms of survival.
  • 2016
  • In: European Journal of Epidemiology. - : Springer Science and Business Media LLC. - 0393-2990 .- 1573-7284. ; 31:5, s. 527-30
  • Journal article (peer-reviewed)abstract
    • Beneficial effects of Mediterranean diet (MD) have been consistently documented. However, to fully understand the public health implications of MD adherence, an informative step is to quantify these effects in terms of survival time differences. The aim of this study was to evaluate the impact of MD on survival, presenting results in terms of differences in median age at death. We used data from 71,333 participants from a large population-based cohort of Swedish men and women, followed-up between January 1, 1998, and December 31, 2012. A total score of MD, ranging from 0 to 8, was calculated by including information on vegetables and fruits consumption, legumes and nuts, non-refined/high fiber grains, fermented dairy products, fish, red meat, use of olive oil/rapeseed oil, and moderate alcohol intake. Multivariable-adjusted differences in median age at death were estimated with Laplace regression and presented as a function of the MD score. During 15 years of follow-up we documented 14,697 deaths. We observed a linear dose-response association between the MD score and median age at death, with higher score associated with longer survival. The difference in median age at death between participants with the extreme scores (0 vs 8) of MD was up to 2 years (23 months, 95 % CI: 16-29). In this study we documented that adherence to MD may accrue benefits up to 2 years of longer survival.
  •  
41.
  • Bellavia, Andrea, et al. (author)
  • Sleep Duration and Survival Percentiles Across Categories of Physical Activity
  • 2014
  • In: American Journal of Epidemiology. - : Oxford University Press (OUP). - 0002-9262 .- 1476-6256. ; 179:4, s. 484-491
  • Journal article (peer-reviewed)abstract
    • The association between long sleep duration and death is not fully understood. Long sleep is associated with low physical activity, which is a strong predictor of death. Our aim was to investigate the association between sleep duration and death across categories of total physical activity in a large prospective cohort of Swedish men and women. We followed a population-based cohort of 70,973 participants (37,846 men and 33,127 women), aged 45-83 years, from January 1998 to December 2012. Sleep duration and physical activity levels were assessed through a questionnaire. We evaluated the association of interest in terms of mortality rates by estimating hazard ratios with Cox regression and in terms of survival by evaluating 15th survival percentile differences with Laplace regression. During 15 years of follow-up, we recorded 14,575 deaths (8,436 men and 6,139 women). We observed a significant interaction between sleep duration and physical activity in predicting death (P < 0.001). Long sleep duration (>8 hours) was associated with increased mortality risk (hazard ratio = 1.24; 95% confidence interval: 1.11, 1.39) and shorter survival (15th percentile difference = -20 months; 95% confidence interval: -30, -11) among only those with low physical activity. The association between long sleep duration and death might be partly explained by comorbidity with low physical activity.
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42.
  • Bellavia, Andrea, et al. (author)
  • Using Laplace Regression to Model and Predict Percentiles of Age at Death When Age Is the Primary Time Scale
  • 2015
  • In: American Journal of Epidemiology. - : OXFORD UNIV PRESS INC. - 0002-9262 .- 1476-6256. ; 182:3, s. 271-277
  • Journal article (peer-reviewed)abstract
    • Increasingly often in epidemiologic research, associations between survival time and predictors of interest are measured by differences between distribution functions rather than hazard functions. For example, differences in percentiles of survival time, expressed in absolute time units (e.g., weeks), may complement the popular risk ratios, which are unitless measures. When analyzing time to an event of interest (e.g., death) in prospective cohort studies, the time scale can be set to start at birth or at study entry. The advantages of one time origin over the other have been thoroughly explored for the estimation of risks but not for the estimation of survival percentiles. In this paper, we analyze the use of different time scales in the estimation of survival percentiles with Laplace regression. Using this regression method, investigators can estimate percentiles of survival time over levels of an exposure of interest while adjusting for potential confounders. Our findings may help to improve modeling strategies and ease interpretation in the estimation of survival percentiles in prospective cohort studies.
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43.
  • Benetou, Vassiliki, et al. (author)
  • Fruit and Vegetable Intake and Hip Fracture Incidence in Older Men and Women : The CHANCES Project
  • 2016
  • In: Journal of Bone and Mineral Research. - : Wiley. - 0884-0431 .- 1523-4681. ; 31:9, s. 1743-1752
  • Journal article (peer-reviewed)abstract
    • The role of fruit and vegetable intake in relation to fracture prevention during adulthood and beyond is not adequately understood. We investigated the potential association between fruit and vegetable intake and hip fracture incidence in a large sample of elderly from Europe and United States. A total of 142,018 individuals (among which 116,509 women), aged ≥60 years old, from five cohorts, were followed-up prospectively for 1,911,482 person-years accumulating 5,552 hip fractures. Fruit and vegetable intake was assessed by validated, cohort-specific, food-frequency questionnaires. Ηip fractures were ascertained through national patient registers or telephone interviews/questionnaires. Adjusted hazard ratios (HR) derived by Cox proportional-hazards regression were estimated for each cohort and subsequently pooled using random-effects meta-analysis. Intake of ≤ 1 servings/day of fruit and vegetables combined was associated with 39% higher hip fracture risk [pooled adjusted HR:1.39, 95% Confidence Intervals (CIs): 1.20, 1.58] in comparison to moderate intake (>3 and ≤5 servings/day) (pfor heterogeneity  = 0.505), whereas higher intakes (>5 servings/day) were not associated with lower risk in comparison to the same reference. Associations were more evident among women. We concluded that a daily intake of one or less servings of fruits and vegetables was associated with increased hip fracture risk in relation to moderate daily intakes. Older adults with such low fruit and vegetable consumption may benefit from raising their intakes to moderate amounts in order to reduce their hip fracture risk. 
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44.
  • Benetou, V., et al. (author)
  • Mediterranean diet and hip fracture incidence among older adults : the CHANCES project
  • 2018
  • In: Osteoporosis International. - : Springer. - 0937-941X .- 1433-2965. ; 29:7, s. 1591-1599
  • Journal article (peer-reviewed)abstract
    • The association between adherence to Mediterranean diet (MD) and hip fracture incidence is not yet established. In a diverse population of elderly, increased adherence to MD was associated with lower hip fracture incidence. Except preventing major chronic diseases, adhering to MD might have additional benefits in lowering hip fracture risk.INTRODUCTION: Hip fractures constitute a major public health problem among older adults. Latest evidence links adherence to Mediterranean diet (MD) with reduced hip fracture risk, but still more research is needed to elucidate this relationship. The potential association of adherence to MD with hip fracture incidence was explored among older adults.METHODS: A total of 140,775 adults (116,176 women, 24,599 men) 60 years and older, from five cohorts from Europe and the USA, were followed-up for 1,896,219 person-years experiencing 5454 hip fractures. Diet was assessed at baseline by validated, cohort-specific, food-frequency questionnaires, and hip fractures were ascertained through patient registers or telephone interviews/questionnaires. Adherence to MD was evaluated by a scoring system on a 10-point scale modified to be applied also to non-Mediterranean populations. In order to evaluate the association between MD and hip fracture incidence, cohort-specific hazard ratios (HR), adjusted for potential confounders, were estimated using Cox proportional-hazards regression and pooled estimates were subsequently derived implementing random-effects meta-analysis.RESULTS: A two-point increase in the score was associated with a significant 4% decrease in hip fracture risk (pooled adjusted HR 0.96; 95% confidence interval (95% CI) 0.92-0.99, pheterogeneity = 0.446). In categorical analyses, hip fracture risk was lower among men and women with moderate (HR 0.93; 95% CI 0.87-0.99) and high (HR 0.94; 95% CI 0.87-1.01) adherence to the score compared with those with low adherence.CONCLUSIONS: In this large sample of older adults from Europe and the USA, increased adherence to MD was associated with lower hip fracture incidence.
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45.
  • Berg, Christina, 1963, et al. (author)
  • Eating patterns and portion size associated with obesity in a Swedish population.
  • 2009
  • In: Appetite. - : Elsevier BV. - 1095-8304 .- 0195-6663. ; 52:1, s. 21-6
  • Journal article (peer-reviewed)abstract
    • The objective of this study was to describe the association between meal pattern and obesity. The study is based on data from the INTERGENE research programme, and the study population consists of randomly selected women and men, aged 25-74, living in the V?stra G?taland Region in Sweden. A total of 3610 were examined. Participants with measured BMI>/=30 were compared with others (BMI<30) with respect to questionnaire data on habitual meal patterns and intake of energy estimated from food frequencies and standard portions. Odds ratios (OR) with 95% confidence intervals were adjusted for age, sex, smoking and physical activity in logistic regression models. Being obese was significantly associated with omitting breakfast, OR 1.41 (1.05-1.90), omitting lunch OR 1.31 (1.04-1.66) and eating at night OR 1.62 (1.10-2.39). Obesity was also related to significantly larger self-reported portion sizes of main meals. No statistically significant relationship with intake of total energy was revealed. Thus, the results indicate that examination of meal patterns and portion sizes might tell us more about obesogenic food patterns than traditional nutrient analyses of food frequencies. Being obese was associated with a meal pattern shifted to later in the day and significantly larger self-reported portions of main meals.
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46.
  • Berg, Christina, 1963, et al. (author)
  • Food patterns and cardiovascular disease risk factors: the Swedish INTERGENE research program.
  • 2008
  • In: The American journal of clinical nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 88:2, s. 289-97
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Analyzing the impact of the intake of many foods simultaneously provides additional knowledge about analyses of nutrients and might make it easier to implement recommendations for the public. OBJECTIVE: The objective was to examine food patterns in a Swedish population and determine how they are related to metabolic risk factors for cardiovascular disease. DESIGN: The study is based on data from the INTERGENE population study of women and men aged 25-74 y in western Sweden. Dietary patterns were identified with cluster analysis of 93 food frequencies reported by 3452 participants. Associations with features of the metabolic syndrome, including blood lipids, blood pressure, and anthropometric measures, were analyzed. RESULTS: Five distinct food patterns were identified, of which one was interpreted as a "healthy" reference pattern. This healthy cluster was distinguished by more frequent consumption of high-fiber and low-fat foods and lower consumption of products rich in fat and sugar. The 4 other clusters differed significantly from the reference cluster with respect to prevalence of cardiovascular disease risk factors and the metabolic syndrome. For example, body mass index and waist-to-hip ratio were significantly higher in a cluster characterized by high consumption of energy-dense drinks and white bread and low consumption of fruit and vegetables (P < 0.0001 and P = 0.004, respectively). CONCLUSIONS: It is possible to distinguish food patterns that are related to obesity and obesity-related cardiovascular disease risk factors in contrast with a more healthy pattern conforming with current dietary guidelines. Thus, the results indicate no reason for questioning the current recommendations.
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47.
  • Bergkvist, Charlotte, et al. (author)
  • Dietary exposure to polychlorinated biphenyls and risk of myocardial infarction - A population-based prospective cohort study
  • 2015
  • In: International Journal of Cardiology. - : ELSEVIER IRELAND LTD. - 0167-5273 .- 1874-1754. ; 183, s. 242-248
  • Journal article (peer-reviewed)abstract
    • Background: Fish consumption may promote cardiovascular health. The role of major food contaminants, such as polychlorinated biphenyls (PCBs) common in fatty fish, is unclear. We assessed the association between dietary PCB exposure and risk of myocardial infarction taking into account the intake of long-chain omega-3 fish fatty acids. Methods: In the prospective population-based Swedish Mammography Cohort, 33,446 middle-aged and elderly women, free from cardiovascular disease, cancer and diabetes at baseline (1997) were followed-up for 12 years. Validated estimates of dietary PCB exposure and intake of fish fatty acids (eicosapentaenoic acid and docosahexaenoic acid; EPA-DHA) were obtained via a food frequency questionnaire at baseline. Results: During follow-up 1386 incident cases of myocardial infarction were ascertained through register-linkage. Women in the highest quartile of dietary PCB exposure (median 286 ng/day) had a multivariable-adjusted RR of myocardial infarction of 1.21 (95% confidence interval [CI], 1.01-1.45) compared to the lowest quartile (median 101 ng/day) before, and 1.58 (95% CI, 1.10-2.25) after adjusting for EPA-DHA. Stratification by low and high EPA-DHA intake, resulted in RRs 2.20 (95% CI, 1.18-4.12) and 1.73 (95% CI, 0.81-3.69), respectively comparing highest PCB tertile with lowest. The intake of dietary EPA-DHA was inversely associated with risk of myocardial infarction after but not before adjusting for dietary PCB. Conclusion: Exposure to PCBs was associated with increased risk of myocardial infarction, while some beneficial effect was associated with increasing EPA and DHA intake. To increase the net benefits of fish consumption, PCB contamination should be reduced to a minimum. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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48.
  • Bergkvist, Charlotte, et al. (author)
  • Dietary exposure to polychlorinated biphenyls and risk of myocardial infarction in men - A population-based prospective cohort study
  • 2016
  • In: Environment International. - : PERGAMON-ELSEVIER SCIENCE LTD. - 0160-4120 .- 1873-6750. ; 88, s. 9-14
  • Journal article (peer-reviewed)abstract
    • Background: Major food contaminants such as polychlorinated biphenyls (PCBs) are proposed to play a role in the etiology of cardiovascular disease (CVD), but to date the impact of PCBs on cardiovascular health need to be explored. Methods and results: We assessed the association between validated food frequency questionnaire-based estimates of dietary PCB exposure and risk of myocardial infarction, ascertained through register-linkage, among 36,759 men from the population-based Swedish Cohort of Men, free of cardiovascular disease, diabetes and cancer at baseline (1997). Relative risks were adjusted for known cardiovascular risk factors, long-chain omega-3 fatty acids (eicosapentaenoic and docosahexaenoic acids) and methyl mercury exposure. During 12 years of follow-up (433,243 person-years), we ascertained 3005 incident cases of myocardial infarction (654 fatal). Compared with the lowest quintile of dietary PCB exposure (median 113 ng/day), men in the highest quintile (median 436 ng/day) had multivariable-adjusted relative risks of 1.74 (95% confidence interval [CI], 1.30-2.33; p-trend < 0.001) for total and 1.97 (95% C11.42-2.75; p-trend < 0.001) for non-fatal myocardial infarction. In mutually adjusted models, dietary PCB exposure was associated with an increased risk of myocardial infarction, while the intake of long-chain omega-3 fish fatty acids was associated with a decreased risk. We also observed an effect modification by adiposity on the association between of dietary PCB exposure and myocardial infarction, with higher risk among lean men (p value for interaction = 0.03). Conclusions: Exposure to PCBs via diet was associated with increased risk of myocardial infarction in men. (C) 2015 Elsevier Ltd. All rights reserved.
  •  
49.
  • Bergkvist, Charlotte, et al. (author)
  • Validation of questionnaire-based long-term dietary exposure to polychlorinated biphenyls using biomarkers
  • 2012
  • In: Molecular Nutrition & Food Research. - : Wiley. - 1613-4125 .- 1613-4133. ; 56:11, s. 1748-1754
  • Journal article (peer-reviewed)abstract
    • Scope The health consequences of lifelong low-level exposure to polychlorinated biphenyls (PCBs) via food are largely unknown, mainly due to the lack of large population-based prospective studies addressing this issue. We validated long-term food frequency questionnaire (FFQ)-based dietary PCB exposure against concentrations of six PCB congeners in serum. Methods and results Dietary PCB exposure was estimated in the Swedish Mammography Cohort by constructing a recipe-based database of CB-153, an indicator for total PCBs in food. The Spearman rank correlation (adjusted for within-person variability) was assessed between concurrent (20042006), past (1997), and long-term (mean of 1997 and 20042006) FFQ-based dietary PCB exposure, respectively, and the following serum PCB congeners, CB-118, CB-138, CB-153, CB-156, CB-170, and CB-180, in women (5685 years of age, n = 201). The correlation between FFQ-based dietary PCB exposure and serum CB-153 was 0.41 (p < 0.001) for the concurrent (median 1.6 ng/kg body weight) and 0.34 (p < 0.05) for the past (median 2.6 ng/kg body weight) exposure assessment. Long-term validity of FFQ-based PCB estimates and the six serum PCB congeners ranged from 0.30 to 0.58 (p < 0.05). Conclusion FFQ-based PCB exposure estimates show acceptable validity in relation to PCB concentrations in serum, justifying their use in large-scale epidemiological studies.
  •  
50.
  • Bien, Stephanie A., et al. (author)
  • Genetic variant predictors of gene expression provide new insight into risk of colorectal cancer
  • 2019
  • In: Human Genetics. - : Springer. - 0340-6717 .- 1432-1203. ; 138:4, s. 307-326
  • Journal article (peer-reviewed)abstract
    • Genome-wide association studies have reported 56 independently associated colorectal cancer (CRC) risk variants, most of which are non-coding and believed to exert their effects by modulating gene expression. The computational method PrediXcan uses cis-regulatory variant predictors to impute expression and perform gene-level association tests in GWAS without directly measured transcriptomes. In this study, we used reference datasets from colon (n=169) and whole blood (n=922) transcriptomes to test CRC association with genetically determined expression levels in a genome-wide analysis of 12,186 cases and 14,718 controls. Three novel associations were discovered from colon transverse models at FDR0.2 and further evaluated in an independent replication including 32,825 cases and 39,933 controls. After adjusting for multiple comparisons, we found statistically significant associations using colon transcriptome models with TRIM4 (discovery P=2.2x10(-4), replication P=0.01), and PYGL (discovery P=2.3x10(-4), replication P=6.7x10(-4)). Interestingly, both genes encode proteins that influence redox homeostasis and are related to cellular metabolic reprogramming in tumors, implicating a novel CRC pathway linked to cell growth and proliferation. Defining CRC risk regions as one megabase up- and downstream of one of the 56 independent risk variants, we defined 44 non-overlapping CRC-risk regions. Among these risk regions, we identified genes associated with CRC (P<0.05) in 34/44 CRC-risk regions. Importantly, CRC association was found for two genes in the previously reported 2q25 locus, CXCR1 and CXCR2, which are potential cancer therapeutic targets. These findings provide strong candidate genes to prioritize for subsequent laboratory follow-up of GWAS loci. This study is the first to implement PrediXcan in a large colorectal cancer study and findings highlight the utility of integrating transcriptome data in GWAS for discovery of, and biological insight into, risk loci.
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