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- Beral, V., et al.
(författare)
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Ovarian Cancer and Body Size : Individual Participant Meta-Analysis Including 25,157 Women with Ovarian Cancer from 47 Epidemiological Studies
- 2012
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Ingår i: PLoS Medicine. - : PUBLIC LIBRARY SCIENCE. - 1549-1277 .- 1549-1676. ; 9:4
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Tidskriftsartikel (refereegranskat)abstract
- Background: Only about half the studies that have collected information on the relevance of women's height and body mass index to their risk of developing ovarian cancer have published their results, and findings are inconsistent. Here, we bring together the worldwide evidence, published and unpublished, and describe these relationships. Methods and Findings: Individual data on 25,157 women with ovarian cancer and 81,311 women without ovarian cancer from 47 epidemiological studies were collected, checked, and analysed centrally. Adjusted relative risks of ovarian cancer were calculated, by height and by body mass index. Ovarian cancer risk increased significantly with height and with body mass index, except in studies using hospital controls. For other study designs, the relative risk of ovarian cancer per 5 cm increase in height was 1.07 (95% confidence interval [CI], 1.05-1.09; p<0.001); this relationship did not vary significantly by women's age, year of birth, education, age at menarche, parity, menopausal status, smoking, alcohol consumption, having had a hysterectomy, having first degree relatives with ovarian or breast cancer, use of oral contraceptives, or use of menopausal hormone therapy. For body mass index, there was significant heterogeneity (p<0.001) in the findings between ever-users and never-users of menopausal hormone therapy, but not by the 11 other factors listed above. The relative risk for ovarian cancer per 5 kg/m(2) increase in body mass index was 1.10 (95% CI, 1.07-1.13; p<0.001) in never-users and 0.95 (95% CI, 0.92-0.99; p = 0.02) in ever-users of hormone therapy. Conclusions: Ovarian cancer is associated with height and, among never-users of hormone therapy, with body mass index. In high-income countries, both height and body mass index have been increasing in birth cohorts now developing the disease. If all other relevant factors had remained constant, then these increases in height and weight would be associated with a 3% increase in ovarian cancer incidence per decade.
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| 3. |
- Larsson, S. C., et al.
(författare)
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Red and processed meat consumption and risk of pancreatic cancer : meta-analysis of prospective studies
- 2012
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Ingår i: British Journal of Cancer. - : NATURE PUBLISHING GROUP. - 0007-0920 .- 1532-1827. ; 106:3, s. 603-607
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Whether red and processed meat consumption is a risk factor for pancreatic cancer remains unclear. We conducted a meta-analysis to summarise the evidence from prospective studies of red and processed meat consumption and pancreatic cancer risk. METHODS: Relevant studies were identified by searching PubMed and EMBASE databases through November 2011. Study-specific results were pooled using a random-effects model. RESULTS: Eleven prospective studies, with 6643 pancreatic cancer cases, were included in the meta-analysis. An increase in red meat consumption of 120 g per day was associated with an overall relative risk (RR) of 1.13 (95% confidence interval (CI) = 0.93-1.39; P-heterogeneity <0.001). Red meat consumption was positively associated with pancreatic cancer risk in men (RR = 1.29; 95% CI = 1.08-1.53; P-heterogeneity = 0.28; five studies), but not in women (RR = 0.93; 95% CI = 0.74-1.16; P-heterogeneity = 0.21; six studies). The RR of pancreatic cancer for a 50 g per day increase in processed meat consumption was 1.19 (95% CI 1.04-1.36; P-heterogeneity = 0.46). CONCLUSION: Findings from this meta-analysis indicate that processed meat consumption is positively associated with pancreatic cancer risk. Red meat consumption was associated with an increased risk of pancreatic cancer in men. Further prospective studies are needed to confirm these findings. British Journal of Cancer (2012) 106, 603-607. doi: 10.1038/bjc.2011.585 www.bjcancer.com Published online 12 January 2012 (C) 2012 Cancer Research UK
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| 4. |
- Larsson, S C, et al.
(författare)
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Vitamin B-6 intake, alcohol consumption, and colorectal cancer : A longitudinal population-based cohort of women
- 2005
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Ingår i: Gastroenterology. - Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden. Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Harvard Univ, Sch Med, Channing Lab, Dept Med, Boston, MA 02115 USA. : W B SAUNDERS CO-ELSEVIER INC. - 0016-5085 .- 1528-0012. ; 128:7, s. 1830-1837
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Tidskriftsartikel (refereegranskat)abstract
- Background & Aims: Vitamin 136 has a crucial role in 1-carbon metabolism, which involves DNA synthesis and DNA methylation. Aberrations in these processes have been implicated in colorectal carcinogenesis. We examined the association between long-term dietary vitamin 136 intake and risk of colorectal cancer and whether this association is modified by consumption of alcohol, which may disrupt 1-carbon metabolism. Methods: Our study population comprised 61,433 women in the population-based Swedish Mammography Cohort. The women were aged 40 to 76 years, had no history of cancer, and completed a food-frequency questionnaire at baseline in 1987-1990. Dietary information was updated in 1997. During a mean follow-up of 14.8 years, 805 incident colorectal cancer cases were diagnosed. Results: After controlling for age and other potential confounders, long-term intake of dietary vitamin 136 was significantly inversely associated with risk of colorectal cancer (P value for trend = .002). Compared with women in the lowest quintile of vitamin 136 intake, those in the highest quintile had a 34% lower risk (multivariate rate ratio, 0.66; 95% confidence interval, 0.50-0.86). The association was most pronounced among women with moderate to high alcohol consumption. The multivariate rate ratio of colorectal cancer comparing extreme quintiles of vitamin 136 intake was 0.28 (95% confidence interval, 0.13-0.59) among women who consumed >= 30 g/wk of alcohol (approximately equivalent to 2 drinks per week). Conclusions: Findings of this study suggest that vitamin 136 may play a role in the prevention of colorectal cancer, particularly among women who drink alcohol.
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| 5. |
- Rashidkhani, B., et al.
(författare)
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Alcohol consumption and risk of renal cell carcinoma : a prospective study of Swedish women
- 2005
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Ingår i: International Journal of Cancer. - Hoboken, USA : John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 117:5, s. 848-853
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Tidskriftsartikel (refereegranskat)abstract
- Previous literature, although not consistent, suggests that moderate alcohol consumption might be associated with decreased risk of renal cell carcinoma (RCC) in women. Thus, we examined the association between alcohol intake and the incidence of RCC by analyzing data from the Swedish Mammography Cohort, a population-based prospective cohort of 59,237 women, aged 40-76 years, who, at baseline in 1987-1990, were cancer free and had completed a food-frequency questionnaire including questions about alcohol consumption. Through June 30, 2004, 132 incident cases of RCC were diagnosed. We used the Cox proportional hazards model to estimate age and body mass index (BMI) adjusted rate ratios (RRs) and their 95% confidence intervals (CIs). Women who consumed >4.3 grams per day of alcohol (ethanol) had nonsignificantly lower risk of RCC than did women who consumed <2.5 g/d (RR = 0.71, 95% CI 0.42-1.19); among women > or = 55 years of age at entry into the cohort, corresponding risk estimates were RR = 0.33, 95% CI 0.10-1.05, p for trend = 0.04 and among women with BMI >25 kg/m2, RR = 0.30, 95% CI 0.09-0.97, p for trend = 0.04. Consistent with these findings, women who drank 1 or more servings of total alcoholic beverages per week had lower RCC risk than did women who drank less (RR = 0.62, 95% CI 0.41-0.94); the corresponding estimate for women > or = 55 years of age was RR = 0.44, 95% CI 0.22-0.88. Results from our prospective cohort study of middle-aged and elderly women indicate that moderate alcohol consumption may be associated with decreased risk of RCC.
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| 6. |
- Rashidkhani, B., et al.
(författare)
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Major dietary patterns and risk of renal cell carcinoma in a prospective cohort of Swedish women
- 2005
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Ingår i: Journal of Nutrition. - Bethesda, USA : American Society for Nutrition. - 0022-3166 .- 1541-6100. ; 135:7, s. 1757-1762
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Tidskriftsartikel (refereegranskat)abstract
- Links between specific foods and the risk of renal cell carcinoma (RCC) are not well established. Dietary patterns may be a better predictor of RCC risk. Our aim was to identify and examine major dietary patterns and their relation to the risk of RCC in a large prospective cohort study of Swedish women. Complete dietary information was available from a FFQ from 46,572 women aged 40-76 y at baseline. We conducted factor analysis to identify dietary patterns. Cox proportional hazard models were used to estimate rate ratios (RRs) and 95% CIs. During a mean of 14.3 y of follow-up, we identified 93 cases of RCC. We observed 3 major dietary patterns in the cohort: Healthy (vegetables, tomato, fish, fruits, poultry, whole grains), Western (sweets, processed meat, refined grains, margarine/butter, high-fat dairy products, fried potato, soft drinks, meat) and Drinker (wine, hard liquor, beer, snacks) pattern. Higher Healthy pattern scores were not significantly associated with decreased risk of RCC (highest vs. lowest tertile RR = 0.81; 95% CI 0.45-1.48 and RR = 0.54; 95% CI 0.27-1.10 among women < or = 65 y). There was a suggestion of an inverse association between the Drinker pattern and RCC risk (RR comparing the 2nd and 3rd with the first tertile, 0.56; 95% CI, 0.34-0.95; and 0.72; 95% CI, 0.42-1.22, respectively, P = 0.08 by Wald test); the association was clearer among women < or = 65 y (P = 0.02 by Wald test). Our data suggest an inverse association between Drinker pattern and the risk of RCC.
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| 10. |
- Beral, V., et al.
(författare)
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Ovarian cancer and smoking: individual participant meta-analysis including 28 114 women with ovarian cancer from 51 epidemiological studies
- 2012
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Ingår i: The Lancet Oncology. - 1474-5488. ; 13:9, s. 946-956
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Tidskriftsartikel (refereegranskat)abstract
- Background Smoking has been linked to mucinous ovarian cancer, but its effects on other ovarian cancer subtypes and on overall ovarian cancer risk are unclear, and the findings from most studies with relevant data are unpublished. To assess these associations, we review the published and unpublished evidence. Methods Eligible epidemiological studies were identified by electronic searches, review articles, and discussions with colleagues. Individual participant data for 28 114 women with and 94 942 without ovarian cancer from 51 epidemiological studies were analysed centrally, yielding adjusted relative risks (RRs) of ovarian cancer in smokers compared with never smokers. Findings After exclusion of studies with hospital controls, in which smoking could have affected recruitment, overall ovarian cancer incidence was only slightly increased in current smokers compared with women who had never smoked (RR 1.06, 95% CI 1.01-1.11, p=0.01). Of 17 641 epithelial cancers with specified histology, 2314 (13%) were mucinous, 2360 (13%) endometrioid, 969 (5%) clear-cell, and 9086 (52%) serous. Smoking-related risks varied substantially across these subtypes (p(heterogeneity)<0.0001). For mucinous cancers, incidence was increased in current versus never smokers (1.79, 95% CI 1.60-2.00, p<0.0001), but the increase was mainly in borderline malignant rather than in fully malignant tumours (2.25, 95% CI 1.91-2.65 vs 1.49, 1.28-1.73; p(heterogeneity)=0.01; almost half the mucinous tumours were only borderline malignant). Both endometrioid (0.81, 95% CI 0.72-0.92, p=0.001) and clear-cell ovarian cancer risks (0.80, 95% CI 0.65-0.97, p=0.03) were reduced in current smokers, and there was no significant association for serous ovarian cancers (0.99, 95% CI 0.93-1.06, p=0.8). These associations did not vary significantly by 13 sociodemographic and personal characteristics of women including their body-mass index, parity, and use of alcohol, oral contraceptives, and menopausal hormone therapy. Interpretation The excess of mucinous ovarian cancers in smokers, which is mainly of tumours of borderline malignancy, is roughly counterbalanced by the deficit of endometrioid and clear-cell ovarian cancers. The substantial variation in smoking-related risks by tumour subtype is important for understanding ovarian carcinogenesis.
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