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1.
  • Grote, Verena A., et al. (författare)
  • The association of circulating adiponectin levels with pancreatic cancer risk: A study within the prospective EPIC cohort
  • 2012
  • Ingår i: International Journal of Cancer. - John Wiley and Sons Inc.. - 0020-7136. ; 130:10, s. 2428-2437
  • Tidskriftsartikel (refereegranskat)abstract
    • Excess body weight and type 2 diabetes mellitus, risk factors of pancreatic cancer, are characterized by decreased levels of adiponectin. In addition to anti-inflammatory and anti-proliferative actions, adiponectin has an important role in regulating glucose metabolism, i.e., decreasing circulating blood glucose levels. Prospectively, hyperglycemia has been associated with risk of pancreatic cancer. The aim of this study was to investigate the association of pre-diagnostic adiponectin levels with pancreatic cancer risk. We conducted a casecontrol study nested within European Prospective Investigation into Cancer and Nutrition. Blood samples of 452 pancreatic cancer cases and 452 individually matched controls were analyzed by immunoassays. Multivariate conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI). Overall, adiponectin showed no association with pancreas cancer risk; however, among never smokers, higher circulating levels of adiponectin were associated with a reduction in pancreatic cancer risk (OR = 0.44 [95% CI 0.230.82] for highest vs. lowest quartile), whereas among current smokers there was no significant association (OR = 1.59 [95% CI 0.673.76] for highest vs. lowest quartile; p-trend = 0.530; p-interaction = 0.309). In our study, lower adiponectin concentrations may be associated with the development of pancreatic cancer among never smokers, whereas the only other prospective study being conducted so far showed a decrease in risk among male smokers. Therefore, further studies are needed to clarify the role of adiponectin in pancreatic cancer development.
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2.
  • Merritt, Melissa A, et al. (författare)
  • Dietary fat intake and risk of epithelial ovarian cancer in the European Prospective Investigation into Cancer and Nutrition.
  • 2014
  • Ingår i: Cancer Epidemiology. - Elsevier. - 1877-7821. ; 38:5, s. 528-537
  • Tidskriftsartikel (refereegranskat)abstract
    • There are inconsistent and limited data available to assess the relationship between fat intake and risk of epithelial ovarian cancer (EOC). We examined the consumption of total fat, fat sources and fat subtypes in relation to risk of EOC and its major histologic subtypes in the European Prospective Investigation into Cancer and Nutrition which includes incident invasive (n=1095) and borderline (n=96) EOC. Cox proportional hazards regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). In multivariate models, we observed no association with consumption of total fat, animal or plant fat, saturated fat, cholesterol, monounsaturated fat, or fatty fish and risk of invasive EOC. There was, however, an increased risk of invasive EOC in the highest category of intake (Quartile 4 vs. Quartile 1) of polyunsaturated fat (HR=1.22, 95% CI=1.02-1.48, Ptrend=0.02). We did not observe heterogeneity in the risk associations in comparisons of serous and endometrioid histologic subtypes. This study does not support an etiological role for total fat intake in relation to EOC risk; however, based on observations of a positive association between intake of polyunsaturated fat and invasive EOC risk in the current and previous studies, this fat subtype warrants further investigation to determine its potential role in EOC development.
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3.
  • Ose, Jennifer, et al. (författare)
  • Endogenous androgens and risk of epithelial invasive ovarian cancer by tumor characteristics in the European Prospective Investigation into Cancer and Nutrition
  • 2014
  • Ingår i: International Journal of Cancer. - John Wiley and Sons Inc.. - 0020-7136. ; 136:2, s. 399-410
  • Tidskriftsartikel (refereegranskat)abstract
    • The role of endogenous androgens and sex hormone-binding globulin (SHBG) in ovarian carcinogenesis is poorly understood. Epithelial invasive ovarian cancer (EOC) is a heterogeneous disease and there are no prospective data on endogenous androgens and EOC risk by tumor characteristics (histology, grade, stage) or the dualistic model of ovarian carcinogenesis (i.e. type I vs. type II, leading to less or more aggressive tumors). We conducted a nested case-control study in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort evaluating androgens and SHBG and invasive EOC risk by tumor characteristics. Female participants who provided a blood sample and were not using exogenous hormones at blood donation were eligible (n = 183,257). A total of 565 eligible women developed EOC; two controls (n = 1,097) were matched per case. We used multivariable conditional logistic regression models. We observed no association between androgens, SHBG and EOC overall. A doubling of androstenedione reduced risk of serous carcinomas by 21% (odds ratio (OR)log2=0.79, 95% confidence interval [CI]=[0.64-0.97]). Moreover, associations differed for low-grade and high-grade carcinomas, with positive associations for low-grade and inverse associations for high-grade carcinomas (e.g. androstenedione: low grade: ORlog2=1.99 [0.98-4.06]; high grade: ORlog2=0.75 [0.61-0.93], p(het)0.01), similar associations were observed for type I/II tumors. This is the first prospective study to evaluate androgens, SHBG and EOC risk by tumor characteristics and type I/II status. Our findings support a possible role of androgens in ovarian carcinogenesis. Additional studies exploring this association are needed. What's new? There appear to be several types of epithelial invasive ovarian cancer (EOC), and hormone-related risk factors are poorly understood. In this study, the authors found that the impact of endogenous androgens on the risk of developing EOC differed depending upon tumor characteristics. Androgen concentrations were positively associated with the risk of low-grade and type-I carcinomas, but the study found an inverse association for high-grade tumors. These findings support a possible role for androgens in ovarian carcinogenesis, and emphasize the need for additional research.
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4.
  • Ricceri, Fulvio, et al. (författare)
  • Risk of second primary malignancies in women with breast cancer: Results from the European prospective investigation into cancer and nutrition (EPIC)
  • 2015
  • Ingår i: International Journal of Cancer. - John Wiley and Sons Inc.. - 0020-7136. ; 137:4, s. 940-948
  • Tidskriftsartikel (refereegranskat)abstract
    • Women with a diagnosis of breast cancer are at increased risk of second primary cancers, and the identification of risk factors for the latter may have clinical implications. We have followed-up for 11 years 10,045 women with invasive breast cancer from a European cohort, and identified 492 second primary cancers, including 140 contralateral breast cancers. Expected and observed cases and Standardized Incidence Ratios (SIR) were estimated using Aalen-Johansen Markovian methods. Information on various risk factors was obtained from detailed questionnaires and anthropometric measurements. Cox proportional hazards regression models were used to estimate the role of risk factors. Women with breast cancer had a 30% excess risk for second malignancies (95% confidence interval-CI 18-42) after excluding contralateral breast cancers. Risk was particularly elevated for colorectal cancer (SIR, 1.71, 95% CI 1.43-2.00), lymphoma (SIR 1.80, 95% CI 1.31-2.40), melanoma (2.12; 1.63-2.70), endometrium (2.18; 1.75-2.70) and kidney cancers (2.40; 1.57-3.52). Risk of second malignancies was positively associated with age at first cancer, body mass index and smoking status, while it was inversely associated with education, post-menopausal status and a history of full-term pregnancy. We describe in a large cohort of women with breast cancer a 30% excess of second primaries. Among risk factors for breast cancer, a history of full-term pregnancy was inversely associated with the risk of second primary cancer. What's new? For the first time, researchers have used cohort data to show that people who survive breast cancer have a higher risk of developing another cancer later. By collecting data on 10,000 breast cancer patients over 11 years, these authors calculated a 30% boost in the patients' risk of developing a second primary malignancy, particularly colorectal cancer, lymphoma, melanoma, endometrial cancer, and kidney cancer. These findings, plus the data they collected on risk factors such as age, smoking, body mass index, and others, will help guide clinicians in screening procedures and follow up care for breast cancer patients.
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5.
  • Sieri, Sabina, et al. (författare)
  • Dietary Fat Intake and Development of Specific Breast Cancer Subtypes.
  • 2014
  • Ingår i: Journal of the National Cancer Institute. - Oxford University Press. - 1460-2105. ; 106:5, s. 068-068
  • Tidskriftsartikel (refereegranskat)abstract
    • We prospectively evaluated fat intake as predictor of developing breast cancer (BC) subtypes defined by estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor 2 receptor (HER2), in a large (n = 337327) heterogeneous cohort of women, with 10062 BC case patients after 11.5 years, estimating BC hazard ratios (HRs) by Cox proportional hazard modeling. High total and saturated fat were associated with greater risk of ER(+)PR(+) disease (HR = 1.20, 95% confidence interval [CI] = 1.00 to 1.45; HR = 1.28, 95% CI = 1.09 to 1.52; highest vs lowest quintiles) but not ER(-)PR(-) disease. High saturated fat was statistically significantly associated with greater risk of HER2(-) disease. High saturated fat intake particularly increases risk of receptor-positive disease, suggesting saturated fat involvement in the etiology of this BC subtype.
6.
  • Travier, Noemie, et al. (författare)
  • Longitudinal changes in weight in relation to smoking cessation in participants of the EPIC-PANACEA study
  • 2012
  • Ingår i: Preventive Medicine. - Elsevier. - 1096-0260. ; 54:3-4, s. 183-192
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose. We assessed the association between smoking cessation and prospective weight change in the European population of the European Prospective Investigation into Cancer and Nutrition-Physical Activity, Nutrition, Alcohol, Cessation of smoking. Eating out of home And obesity (EPIC-PANACEA) project. Methods. The study involved more than 300,000 healthy volunteers, recruited between 1992 and 2000 in 9 European countries, who provided data on anthropometry and smoking habits at baseline and after a follow-up of 5 years on average. Adjusted mixed-effects linear regression models were used to obtain sex-specific summary estimates of the association between the change in smoking status and the annual change in weight. Results. Smoking cessation tends to be followed by weight gain; when compared to stable smokers, annual weight gain was higher in men (0.44 kg (95%CI: 0.36; 0.52)) and women (0.46 kg (95%CI: 0.41; 0.52)) who stopped smoking during follow-up. When smokers who stopped smoking at least 1 year before recruitment were compared to never smokers, no major differences in annual weight gain were observed. The excess weight gain following smoking cessation appears to mainly occur in the first years following the cessation. Conclusions. When considering the benefits of smoking cessation, such findings strengthen the need for promoting cessation offering information on weight gain control and support to weight-concerned smokers in order to remove a barrier to quitting. (C) 2011 Elsevier Inc. All rights reserved.
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7.
  • Travier, Noemie, et al. (författare)
  • Longitudinal changes in weight in relation to smoking cessation in participants of the EPIC-PANACEA study
  • 2012
  • Ingår i: Preventive Medicine. - Elsevier. - 0091-7435 .- 1096-0260. ; 54:3-4, s. 183-192
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Purpose. We assessed the association between smoking cessation and prospective weight change in the European population of the European Prospective Investigation into Cancer and Nutrition-Physical Activity, Nutrition, Alcohol, Cessation of smoking. Eating out of home And obesity (EPIC-PANACEA) project. Methods. The study involved more than 300,000 healthy volunteers, recruited between 1992 and 2000 in 9 European countries, who provided data on anthropometry and smoking habits at baseline and after a follow-up of 5 years on average. Adjusted mixed-effects linear regression models were used to obtain sex-specific summary estimates of the association between the change in smoking status and the annual change in weight. Results. Smoking cessation tends to be followed by weight gain; when compared to stable smokers, annual weight gain was higher in men (0.44 kg (95%CI: 0.36; 0.52)) and women (0.46 kg (95%CI: 0.41; 0.52)) who stopped smoking during follow-up. When smokers who stopped smoking at least 1 year before recruitment were compared to never smokers, no major differences in annual weight gain were observed. The excess weight gain following smoking cessation appears to mainly occur in the first years following the cessation. Conclusions. When considering the benefits of smoking cessation, such findings strengthen the need for promoting cessation offering information on weight gain control and support to weight-concerned smokers in order to remove a barrier to quitting. (C) 2011 Elsevier Inc. All rights reserved.</p>
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8.
  • Zamora-Ros, Raul, et al. (författare)
  • Energy and macronutrient intake and risk of differentiated thyroid carcinoma in the European Prospective Investigation into Cancer and Nutrition (EPIC) study.
  • 2016
  • Ingår i: International Journal of Cancer. - John Wiley and Sons Inc.. - 0020-7136. ; 138:1, s. 65-73
  • Tidskriftsartikel (refereegranskat)abstract
    • Incidence rates of differentiated thyroid carcinoma (TC) have increased in many countries. Adiposity and dietary risk factors may play a role, but little is known on the influence of energy intake and macronutrient composition. The aim of this study is to investigate associations between TC and the intake of energy, macronutrients, glycemic index (GI) and glycemic load in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. The study included 477,274 middle-age participants (70.2% women) from 10 European countries. Dietary data were collected using country-specific validated dietary questionnaires. Total carbohydrates, proteins, fats, saturated, monounsaturated and polyunsaturated fats (PUFA), starch, sugar, fiber and glycemic load were computed as g/1000kcal. Multivariable Cox regression was used to calculate multivariable adjusted hazard ratios (HR) and 95% confidence interval (CI) by intake quartile (Q). After a mean follow-up time of 11 years, differentiated TC was diagnosed in 556 participants (90% women). Overall, we only found significant associations with total energy (HRQ4vsQ1 1.29; 95% CI 1.00-1.68) and PUFA intakes (HRQ4vsQ1 0.74, 95% CI 0.57-0.95). However, the associations with starch and sugar intake and GI were significantly heterogeneous across BMI groups, i.e., positive associations with starch and GI were found in participants with a body mass index (BMI) ≥25 and with sugar intake in those with BMI <25. Moreover, inverse associations with starch and GI were observed in subjects with BMI<25. In conclusion, our results suggest that high total energy and low PUFA intakes may increase the risk of differentiated TC. Positive associations with starch intake and GI in participants with BMI ≥25 suggest that those persons may have a greater insulin response to high starch intake and GI than lean people. This article is protected by copyright. All rights reserved.
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9.
  • Aleksandrova, Krasimira, et al. (författare)
  • Combined impact of healthy lifestyle factors on colorectal cancer: a large European cohort study
  • 2014
  • Ingår i: BMC Medicine. - BioMed Central (BMC). - 1741-7015. ; 12
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Excess body weight, physical activity, smoking, alcohol consumption and certain dietary factors are individually related to colorectal cancer (CRC) risk; however, little is known about their joint effects. The aim of this study was to develop a healthy lifestyle index (HLI) composed of five potentially modifiable lifestyle factors healthy weight, physical activity, non-smoking, limited alcohol consumption and a healthy diet, and to explore the association of this index with CRC incidence using data collected within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Methods: In the EPIC cohort, a total of 347,237 men and women, 25- to 70-years old, provided dietary and lifestyle information at study baseline (1992 to 2000). Over a median follow-up time of 12 years, 3,759 incident CRC cases were identified. The association between a HLI and CRC risk was evaluated using Cox proportional hazards regression models and population attributable risks (PARs) have been calculated. Results: After accounting for study centre, age, sex and education, compared with 0 or 1 healthy lifestyle factors, the hazard ratio (HR) for CRC was 0.87 (95% confidence interval (CI): 0.44 to 0.77) for two factors, 0.79 (95% CI: 0.70 to 0.89) for three factors, 0.66 (95% CI: 0.58 to 0.75) for four factors and 0.63 (95% CI: 0.54 to 0.74) for five factors; P-trend <0.0001. The associations were present for both colon and rectal cancers, HRs, 0.61 (95% CI: 0.50 to 0.74; P for trend <0.0001) for colon cancer and 0.68 (95% CI: 0.53 to 0.88; P-trend <0.0001) for rectal cancer, respectively (P-difference by cancer sub-site = 0.10). Overall, 16% of the new CRC cases (22% in men and 11% in women) were attributable to not adhering to a combination of all five healthy lifestyle behaviours included in the index. Conclusions: Combined lifestyle factors are associated with a lower incidence of CRC in European populations characterized by western lifestyles. Prevention strategies considering complex targeting of multiple lifestyle factors may provide practical means for improved CRC prevention.
10.
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