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  • 1
    Keywords: RISK ; OBESITY ; COLON-CANCER ; nutrition ; RECTAL-CANCER ; PATIENT SURVIVAL ; PHYSICAL-ACTIVITY ; BODY-MASS INDEX ; TREATMENT-RELATED TOXICITY ; VISCERAL ADIPOSITY
    Abstract: General and abdominal adiposity are associated with a high risk of developing colorectal cancer (CRC), but the role of these exposures on cancer survival has been less studied. The association between pre-diagnostic anthropometric characteristics and CRC-specific and all-cause death was examined among 3,924 men and women diagnosed with CRC between 1992 and 2009 in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Multivariable Cox proportional hazards models were used to calculate hazard ratios (HRs) and corresponding 95% confidence intervals (CIs). Over a mean follow-up period of 49 months, 1,309 deaths occurred of which 1,043 (79.7%) were due to CRC. In multivariable analysis, pre-diagnostic BMI 〉/=30 kg/m(2) was associated with a high risk for CRC-specific (HR = 1.26, 95% CI = 1.04-1.52) and all-cause (HR = 1.32, 95% CI = 1.12-1.56) death relative to BMI 〈25 kg/m(2) . Every 5 kg/m(2) increase in BMI was associated with a high risk for CRC-specific (HR = 1.10, 95% CI = 1.02-1.19) and all-cause death (HR = 1.12, 95% CI = 1.05-1.20); and every 10 cm increase in waist circumference was associated with a high risk for CRC-specific (HR = 1.09, 95% CI = 1.02-1.16) and all-cause death (HR = 1.11, 95% CI = 1.05-1.18). Similar associations were observed for waist-to-hip and waist-to-height ratios. Height was not associated with CRC-specific or all-cause death. Associations tended to be stronger among men than in women. Possible interactions by age at diagnosis, cancer stage, tumour location, and hormone replacement therapy use among postmenopausal women were noted. Pre-diagnostic general and abdominal adiposity are associated with lower survival after CRC diagnosis.
    Type of Publication: Journal article published
    PubMed ID: 24623514
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  • 2
    Keywords: CANCER ; lung cancer ; SUPPORT ; COHORT ; EPIDEMIOLOGY ; MORTALITY ; RISK ; HETEROCYCLIC AMINES ; ASSOCIATION ; WOMEN ; FISH ; DIET ; FAT ; CONSUMPTION ; EPIC ; meat ; CALIBRATION ; DIETARY HABITS ; RECALLS ; HEME IRON ; MUTAGENS
    Abstract: Evidence from case-control studies, but less so from cohort studies, suggests a positive association between meat intake and risk of lung cancer. Therefore, this association was evaluated in the frame of the European Prospective Investigation into Cancer and Nutrition, EPIC. Data from 478,021 participants, recruited from 10 European countries, who completed a dietary questionnaire in 1992-2000 were evaluated; 1,822 incident primary lung cancer cases were included in the present evaluation. Relative risk estimates were calculated for categories of meat intake using multi-variably adjusted Cox proportional hazard models. In addition, the continuous intake variables were calibrated by means of 24-h diet recall data to account for part of the measurement error. There were no consistent associations between meat consumption and the risk of lung cancer. Neither red meat (RR = 1.06, 95% CI 0.89-1.27 per 50 g intake/day; calibrated model) nor processed meat (RR = 1.13, 95% CI 0.95-1.34 per 50 g/day; calibrated model) was significantly related to an increased risk of lung cancer. Also, consumption of white meat and fish was not associated with the risk of lung cancer. These findings do not support the hypothesis that a high intake of red and processed meat is a risk factor for lung cancer
    Type of Publication: Journal article published
    PubMed ID: 21479828
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  • 3
    Keywords: CANCER ; COHORT ; RISK ; IMPACT ; CARCINOGENESIS ; BIOMARKERS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; VARIANTS ; HEALTH ; PLASMA ; AGE ; colorectal cancer ; smoking ; COLORECTAL-CANCER ; FIBER ; COLON-CANCER ; MASS-SPECTROMETRY ; EPIC ; nutrition ; education ; NESTED CASE-CONTROL ; physical activity ; ONCOLOGY ; case-control study ; REGRESSION ; ASSOCIATIONS ; VARIANT ; PHYSICAL-ACTIVITY ; biomarker ; methods ; dietary patterns ; GENOTYPE ; LOCUS ; prospective ; CANCER-RISK ; nested case-control study ; COMMON MUTATION ; MTHFR POLYMORPHISMS ; FOLIC-ACID ; Genetic ; FOLATE STATUS ; METHYLENETETRAHYDROFOLATE REDUCTASE POLYMORPHISM ; nested case control study ; C677T MTHFR POLYMORPHISM ; CARBON METABOLIC PATHWAY ; HUMAN METHIONINE SYNTHASE
    Abstract: Background: A potential dual role of folate in colorectal cancer (CRC) is currently subject to debate. We investigate the associations between plasma folate, several relevant folate-related polymorphisms, and CRC risk within the large European Prospective Investigation into Cancer and Nutrition cohort. Methods: In this nested case-control study, 1,367 incident CRC cases were matched to 2,325 controls for study center, age, and sex. Risk ratios (RR) were estimated with conditional logistic regression and adjusted for smoking, education, physical activity, and intake of alcohol and fiber. Results: Overall analyses did not reveal associations of plasma folate with CRC. The RR (95% confidence interval; P-trend) for the fifth versus the first quintile of folate status was 0.94 (0.74-1.20; 0.44). The polymorphisms MTHFR677C -〉 T, MTHFR1298A -〉 C, MTR2756A -〉 G, MTRR66A -〉 G, and MTHFD11958G -〉 A were not associated with CRC risk. However, in individuals with the lowest plasma folate concentrations, the MTHFR 677TT genotype showed a statistically nonsignificant increased CRC risk [RR (95% CI; P-trend) TT versus CC = 1.39 (0.87-2.21); 0.12], whereas those with the highest folate concentrations showed a nonsignificant decreased CRC risk [RR TT versus CC = 0.74 (0.39-1.37); 0.34]. The SLC19A180G -〉 A showed a positive association with CRC risk [RR AA versus GG 1.30 (1.06-1.59); 〈0.01]. Conclusions: This large European prospective multicenter study did not show an association of CRC risk with plasma folate status nor with MTHFR polymorphisms. Impact: Findings of the present study tend to weaken the evidence that folate plays an important role in CRC carcinogenesis. However, larger sample sizes are needed to adequately address potential gene-environment interactions. Cancer Epidemiol Biomarkers Prev; 19(5); 1328-40. (C)2010 AACR
    Type of Publication: Journal article published
    PubMed ID: 20447924
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