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Träfflista för sökning "swepub ;lar1:(umu);pers:(Riboli Elio);pers:(Chirlaque Maria Dolores);pers:(Khaw Kay Tee);conttype:(refereed);pers:(Manjer Jonas);pers:(Ardanaz Eva)"

Search: swepub > Umeå University > Riboli Elio > Chirlaque Maria Dolores > Khaw Kay Tee > Peer-reviewed > Manjer Jonas > Ardanaz Eva

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  • Dossus, Laure, et al. (author)
  • Reproductive risk factors and endometrial cancer : the European prospective investigation into cancer and nutrition
  • 2010
  • In: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 127:2, s. 442-451
  • Journal article (peer-reviewed)abstract
    • Endometrial cancer risk has been associated with reproductive factors (age at menarche, age at menopause, parity, age at first and last birth, time since last birth and use of oral contraceptives (OCs)]. However, these factors are closely interrelated and whether they act independently still requires clarification. We conducted a study to examine the association of menstrual and reproductive variables with the risk of endometrial cancer among the European Prospective Investigation into Cancer and Nutrition (EPIC). Among the 302,618 women eligible for the study, 1,017 incident endometrial cancer cases were identified. A reduction in endometrial cancer risk was observed in women with late menarche, early menopause, past OC use, high parity and a shorter time since last full-term pregnancy (FTP). No association was observed for duration of breast feeding after adjustment for number of FTP or for abortion (spontaneous or induced). After mutual adjustment, late age at menarche, early age at menopause and duration of OC use showed similar risk reductions of 7-8% per year of menstrual life, whereas the decreased risk associated with cumulative duration of FTPs was stronger (22% per year). In conclusion, our findings confirmed a reduction in risk of endometrial cancer with factors associated with a lower cumulative exposure to estrogen and/or higher exposure to progesterone, such as increasing number of FTPs and shorter menstrual lifespan and, therefore, support an important role of hormonal mechanisms in endometrial carcinogenesis.
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  • Michaud, Dominique S, et al. (author)
  • Coffee and tea intake and risk of brain tumors in the European prospective investigation into cancer and nutrition (EPIC) cohort study
  • 2010
  • In: American Journal of Clinical Nutrition. - : American Society for Nutrition. - 0002-9165 .- 1938-3207. ; 92:5, s. 1145-1150
  • Journal article (peer-reviewed)abstract
    • Background: In a recent US cohort study, total coffee and tea consumption was inversely associated with risk of glioma, and experimental studies showed that caffeine can slow the invasive growth of glioblastoma.Objective: The objective was to examine the relation between coffee and tea intake and the risk of glioma and meningioma in a large European cohort study, the European Prospective Investigation into Cancer and Nutrition (EPIC).Design: Data on coffee and tea intake were collected from men and women recruited into the EPIC cohort study. Over an average of 8.5 y of follow-up, 343 cases of glioma and 245 cases of meningioma were newly diagnosed in 9 countries. We used Cox proportional hazards models to examine the relation between coffee and tea and brain tumors.Results: We observed no associations between coffee, tea, or combined coffee and tea consumption and risk of either type of brain tumor when using quantiles based on country-specific distributions of intake. However, a significant inverse association was observed for glioma risk among those consuming ≥100 mL coffee and tea per day compared with those consuming <100 mL/d (hazard ratio: 0.66; 95% CI: 0.44, 0.97; P = 0.03). The association was slightly stronger in men (hazard ratio: 0.59; 95% CI: 0.34, 1.01) than in women (hazard ratio: 0.74; 95% CI: 0.42, 1.31), although neither was statistically significant.Conclusions: In this large cohort study, we observed an inverse association between total coffee and tea consumption and risk of glioma that was consistent with the findings of a recent study. These findings, if further replicated in other studies, may provide new avenues of research on gliomas.
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  • Pischon, Tobias, et al. (author)
  • Body Size and Risk of Prostate Cancer in the European Prospective Investigation into Cancer and Nutrition
  • 2008
  • In: Cancer Epidemiology Biomarkers & Prevention. - Baltimore : Waverly Press. - 1538-7755 .- 1055-9965. ; 17:11, s. 3252-3261
  • Journal article (peer-reviewed)abstract
    • Background: Body size has been hypothesized to influence the risk of prostate cancer; however, most epidemiologic studies have relied on body mass index (BMI) to assess adiposity, whereas only a few studies have examined whether body fat distribution predicts prostate cancer. Methods: We examined the association of height, BMI, waist and hip circumference, and waist-hip ratio with prostate cancer risk among 129,502 men without cancer at baseline from 8 countries of the European Prospective Investigation into Cancer and Nutrition (EPIC), using Cox regression, with age as time metric, stratifying by study center and age at recruitment, and adjusting for education, smoking status, alcohol consumption, and physical activity. Results: During a mean follow-up of 8.5 years, 2,446 men developed prostate cancer. Waist circumference and waist-hip ratio were positively associated with risk of advanced disease. The relative risk of advanced prostate cancer was 1.06 (95% confidence interval, 1.01-1.1) per 5-cm-higher waist circumference and 1.21 (95% confidence interval, 1.04-1.39) per 0.1-unit-higher waist-hip ratio. When stratified by BMI, waist circumference and waist-hip ratio were positively related to risk of total, advanced, and high-grade prostate cancer among men with lower but not among those with higher BMI (P-interaction for waist with BMI, 0.25, 0.02, and 0.05, respectively; P-interaction for waist-hip ratio with BMI, 0.27, 0.22, and 0.14; respectively). Conclusions: These data suggest that abdominal adiposity may be associated with an increased risk of advanced prostate cancer. This association may be stronger among individuals with lower BMI; however, this finding needs confirmation in future studies. (Cancer Epidemiol Biomarkers Prev 2008;17(11):3252-61)
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  • Rinaldi, Sabina, et al. (author)
  • Glycosylated Hemoglobin and Risk of Colorectal Cancer in Men and Women, the European Prospective Investigation into Cancer and Nutrition
  • 2008
  • In: Cancer Epidemiology Biomarkers & Prevention. - 1538-7755 .- 1055-9965. ; 17:11, s. 3108-3115
  • Journal article (peer-reviewed)abstract
    • Although large-scale prospective cohort studies have related hyperglycemia to increased risk of cancer overall, studies specifically on colorectal cancer have been generally small. We investigated the association between prediagnostic levels of glycosylated hemoglobin (HbA1c), a marker for average glucose level in blood, and colorectal cancer risk in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition cohort. One thousand and twenty-six incident colorectal cancer cases (561 men and 465 women) and 1,026 matched controls were eligible for the study. Multivariate conditional logistic regression was used to estimate odds ratios (ORS) adjusted for possible confounders. Increasing HbA1c percentages were statistically significantly associated with a mild increase in colorectal cancer risk in the whole population [OR, 1.10; 95% confidence interval (CI), 1.01,1.19 for a 10% increase in HbA1c]. In women, increasing HbA1c percentages were associated with a statistically significant increase in colorectal cancer risk (OR, 1.16; 95% CI, 1.01, 1.32 for a 10% increase in HbA1c) and with a borderline statistically significant increase in rectum cancer (OR, 1.22; 95% CI, 0.99,1.50 for a 10% increase in HbA1c). No significant association with cancer risk was observed in men. The results of the current study suggest a mild implication of hyperglycemia in colorectal cancer, which seems more important in women than in men, and more for cancer of the rectum than of the colon. (Cancer Epidemiol Biomarkers Prev 2008;17(11):3108-15)
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