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- Cho, E, et al.
(författare)
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Dairy foods, calcium, and colorectal cancer : A pooled analysis of 10 cohort studies
- 2004
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Ingår i: Journal of the National Cancer Institute. - Harvard Univ, Sch Med, Channing Lab, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA. 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 Publ Hlth, Dept Biostat, Boston, MA 02115 USA. Loma Linda Univ, Ctr Hlth Res, Sch Med, Loma Linda, CA USA. Maastricht Univ, Dept Epidemiol, Maastricht, Netherlands. Harvard Ctr Canc Prevent, Boston, MA USA. Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA. SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY USA. TNO, Nutr & Food Res Inst, Dept Epidemiol, Zeist, Netherlands. Univ Toronto, Fac Med, Dept Publ Hlth Sci, Toronto, ON, Canada. Natl Publ Hlth Inst, Dept Epidemiol & Hlth Promot, Helsinki, Finland. Fred Hutchinson Canc Res Ctr, Canc Prevent Res Program, Seattle, WA USA. Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA. Natl Inst Environm Hlth Sci, Epidemiol Branch, Res Triangle Pk, NC USA. NYU, Dept Obstet Gynecol, Sch Med, New York, NY USA. Natl Inst Environm Med, Div Nutr Epidemiol, Stockholm, Sweden. NYU, Sch Med, Nelson Inst Environm Med & Kaplan Canc Ctr, New York, NY USA. : OXFORD UNIV PRESS INC. - 0027-8874 .- 1460-2105. ; 96:13, s. 1015-1022
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Tidskriftsartikel (refereegranskat)abstract
- Background. Studies in animals have suggested that calcium may reduce the risk of colorectal cancer. However, results from epidemiologic studies of intake of calcium or dairy foods and colorectal cancer risk have been inconclusive. Methods: We pooled the primary data from 10 cohort studies in five countries that assessed usual dietary intake by using a validated food frequency questionnaire at baseline. For most studies, follow-up was extended beyond that in the original publication. The studies included 534 536 individuals, among whom 4992 incident cases of colorectal cancer were diagnosed between 6 and 16 years of follow-up. Pooled multivariable relative risks for categories of milk intake and quintiles of calcium intake and 95% confidence intervals (CIs) were calculated. All statistical tests were two-sided. Results: Milk intake was related to a reduced risk of colorectal cancer. Compared with the lowest category of intake (<70 g/day), relative risks of colorectal cancer for increasing categories (70-174, 175-249, and greater than or equal to250 g/day) of milk intake were 0.94 (95% CI = 0.86 to 1.02), 0.88 (95% CI = 0.81 to 0.96), and 0.85 (95% CI = 0.78 to 0.94), respectively (P-trend<.001). Calcium intake was also inversely related to the risk of colorectal cancer. The relative risk for the highest versus the lowest quintile of intake was 0.86 (95% CI = 0.78 to 0.95; P-trend = .02) for dietary calcium and 0.78 (95% CI = 0.69 to 0.88; P-trend<.001) for total calcium (combining dietary and supplemental sources). These results were consistent across studies and sex. The inverse association for milk was limited to cancers of the distal colon (P-trend<.001) and rectum (P-trend = .02). Conclusion: Higher consumption of milk and calcium is associated with a lower risk of colorectal cancer.
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- Larsson, S C, et al.
(författare)
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Diabetes mellitus and risk of colorectal cancer : A meta-analysis
- 2005
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Ingår i: Journal of the National Cancer Institute. - Natl Inst Environm Med, Div Nutr Epidemiol, Karolinska Inst, SE-17177 Stockholm, Sweden. : OXFORD UNIV PRESS INC. - 0027-8874 .- 1460-2105. ; 97:22, s. 1679-1687
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Tidskriftsartikel (refereegranskat)abstract
- Background: Diabetes has been associated with an increased risk of colorectal cancer in most, but not all, studies. Findings have also been inconclusive with regard to sex and subsite in the colorectum. To resolve these inconsistencies, we conducted a meta-analysis of published data on the association between diabetes and the incidence and mortality of colorectal cancer. Methods: We identified studies by a literature search of Medline from January 1, 1966, through July 31, 2005, and by searching the reference lists of pertinent articles. Summary relative risks (RRs) with 95% confidence intervals (CIs) were calculated with a random-effects model. All statistical tests were two-sided. Results: Analysis of 15 studies (six case-control and nine cohort studies), including 2593935 participants, found that diabetes was associated with an increased risk of colorectal cancer, compared with no diabetes (summary RR of colorectal cancer incidence = 1.30, 95% CI = 1.20 to 1.40), without heterogeneity between studies (P-heterogeneity = .21). These results were consistent between case-control and cohort studies and between studies conducted in the United States and in Europe. The association between diabetes and colorectal cancer incidence did not differ statistically significantly by sex (summary RR among women = 1.33, 95% CI = 1.23 to 1.44; summary RR among men = 1.29, 95% CI = 1.15 to 1.44; P-heterogeneity = .26) or by cancer subsite (summary RR for colon = 1.43, 95% CI = 1.28 to 1.60; summary RR for rectum = 1.33, 95% CI = 1.14 to 1.54; P-heterogeneity = .42). Diabetes was positively associated with colorectal cancer mortality (summary RR = 1.26, 95% CI = 1.05 to 1.50), but there was evidence for heterogeneity between studies (Pheterogeneity = .04). Conclusions: Our findings strongly support a relationship between diabetes and increased risk of colon and rectal cancer in both women and men.
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- Larsson, S C, et al.
(författare)
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Dietary folate intake and incidence of ovarian cancer : The Swedish Mammography Cohort
- 2004
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Ingår i: Journal of the National Cancer Institute. - Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden. Harvard Univ, Sch Med, Boston, MA USA. Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA. Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. : OXFORD UNIV PRESS INC. - 0027-8874 .- 1460-2105. ; 96:5, s. 396-402
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Tidskriftsartikel (refereegranskat)abstract
- Background: Mounting evidence suggests that a low intake of the water-soluble B vitamin folate is associated with breast and colorectal carcinogenesis, especially among alcohol drinkers. However, epidemiologic data specifically linking folate intake to ovarian cancer risk are limited. Methods: We examined the association between dietary folate intake (i.e., folate from food sources) and the incidence of total epithelial ovarian cancer and its subtypes by analyzing data from the Swedish Mammography Cohort, a population-based prospective cohort of 61084 women, aged 38-76 years, who, at baseline (i.e., from 1987 to 1990), were cancer-free and had completed a food-frequency questionnaire. Through June 30, 2003, 266 incident cases of invasive epithelial ovarian cancer were diagnosed. We used Cox proportional hazards models to estimate multivariable relative risks (RRs) of ovarian cancer with 95% confidence intervals (CIs). All statistical tests were two-sided. Results: Overall, dietary folate intake was weakly inversely associated with total epithelial ovarian cancer risk (RR for highest versus lowest quartile of intake = 0.67, 95% CI = 0.43 to 1.04; P-trend =.08). Among women who consumed more than 20 g of alcohol (approximately two drinks) per week, there was a strong inverse association between dietary folate intake and total epithelial ovarian cancer risk (RR for highest versus lowest quartile of intake = 0.26, 95% CI = 0.11 to 0.60; P-trend = .001), but among women who consumed 20 g or less of alcohol per week, there was no such association (RR for highest versus lowest quartile of intake = 1.00, 95% CI = 0.59 to 1.70; P-trend = .80). The absolute risk of epithelial ovarian cancer for the lowest three quartiles versus the highest quartile of folate intake was 8 per 100 000 personyears (95% CI = 0 to 16 per 100000 person-years) overall and 26 per 100 000 person-years (95% CI = 10 to 42 per 100 000 person-years) among those who consumed more than 20 g of alcohol per week. The association between dietary folate intake and cancer risk did not vary substantially among subtypes of epithelial ovarian cancer. Conclusion: A high dietary folate intake may play a role in reducing the risk of ovarian cancer, especially among women who consume alcohol.
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- Larsson, S C, et al.
(författare)
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Folate intake and pancreatic cancer incidence : A prospective study of Swedish women and men
- 2006
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Ingår i: Journal of the National Cancer Institute. - 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. Brigham & Womens Hosp, Channing Lab, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. : OXFORD UNIV PRESS INC. - 0027-8874 .- 1460-2105. ; 98:6, s. 407-413
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Tidskriftsartikel (refereegranskat)abstract
- Background. Epidemiologic evidence supports an association between high folate intake and reduced risk of some cancers, in particular colorectal cancer. However, epidemiologic data concerning the relationship between folate and pancreatic cancer risk are sparse. We examined the association between folate intake and risk of pancreatic cancer in a population-based prospective study of Swedish women and men. Methods: We prospectively followed 81922 women and men in the Swedish Mammography Cohort and the Cohort of Swedish Men who were cancer-free and completed a 96-item food-frequency questionnaire in 1997. Cox proportional hazards models were used to estimate multivariable rate ratios (RRs) with 95% confidence intervals (CIs). All statistical tests were two-sided. Results: A total of 135 incident pancreatic cancer cases were diagnosed during a mean follow-up of 6.8 years. In multivariable analyses controlling for age, smoking, fruit and vegetable consumption, and other potential confounders, dietary and total folate intakes were statistically significantly inversely associated with risk of pancreatic cancer. The multivariable rate ratios of pancreatic cancer for those in the highest category of folate intake (>= 350 mu g/day) compared with the lowest category of intake (< 200 mu g/day) were 0.25 (95% CI = 0.11 to 0.59; P-trend = .002) for dietary folate and 0.33 (95% CI = 0.15 to 0.72; P-trend = .01) for total folate (combining dietary and supplemental sources). Folic acid from supplements was not associated with pancreatic cancer (for >= 300 mu g/day compared with 0 mu g/day of supplemental folic acid, multivariable RR = 1.02; 95% CI = 0.56 to 1.88). The sex- and age-standardized incidence rates of pancreatic cancer per 100000 person-years were 41 for the lowest and 18 for the highest category of dietary folate intake. Conclusion: Our results suggest that increased intake of folate from food sources, but not from supplements, may be associated with a reduced risk of pancreatic cancer.
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| 7. |
- Larsson, SC, et al.
(författare)
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Folate and risk of breast cancer: a meta-analysis
- 2007
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Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 1460-2105 .- 0027-8874. ; 99:1, s. 64-76
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Tidskriftsartikel (refereegranskat)
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| 10. |
- Suzuki, R, et al.
(författare)
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Alcohol and postmenopausal breast cancer risk defined by estrogen and progesterone receptor status : A prospective cohort study
- 2005
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Ingår i: Journal of the National Cancer Institute. - Karolinska Inst, Div Nutr Epidemiol, Natl Inst Environm Med, Dept Med Epidemiol & Biostat, S-17177 Stockholm, Sweden. Tokyo Metropolitan Komagome Hosp, Dept Surg & Breast Oncol, Tokyo Metropolitan Canc & Infect Dis Ctr, Tokyo, Japan. Harvard Univ, Sch Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA. : OXFORD UNIV PRESS INC. - 0027-8874 .- 1460-2105. ; 97:21, s. 1601-1608
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Tidskriftsartikel (refereegranskat)abstract
- Background: Alcohol intake has been reported to be positively associated with an increased risk of postmenopausal breast cancer; however, the association with the estrogen receptor (ER) and progesterone receptor (PR) status of the breast tumors remains unclear. Methods: Self-reported data on alcohol consumption were collected in 1987 and 1997 from 51847 postmenopausal women in the population-based Swedish Mammography Cohort. Through June 30,2004,1188 invasive breast cancer case patients with known ER and PR status were identified during an average 8.3-year follow-up. We used Cox proportional hazards models to estimate multivariable relative risks (RRs) of breast cancer, adjusting for age; family history of breast cancer; body mass index; height; parity; age at menarche, first birth, and menopause; education level; use of postmenopausal hormones; and diet. Heterogeneity among groups was evaluated using the Wald test. All statistical tests were two-sided. Results: Alcohol consumption was associated with an increased risk for the development of ER-positive (+) tumors, irrespective of PR status (highest intake [ >= 10 g of alcohol per day] versus nondrinkers, multivariable RR = 1.35, 95% confidence interval [CI] = 1.02 to 1.80; P-trend < .049 for ER+PR+ tumors; and RR = 2.36, 95% CI = 1.56 to 3.56; P-trend < .001 for ER+PR-tumors). The absolute rate of ER+ breast cancer (standardized to the age distribution of person-years experienced by all study participants using 5-year age categories) was 232 per 100000 person-years among women in the highest category of alcohol intake, and 158 per 100000 person-years among nondrinkers. No association was observed between alcohol intake and the risk of developing ER-tumors. Furthermore, we observed a statistically significant interaction between alcohol intake and the use of postmenopausal hormones on the risk for ER+PR+ tumors (P-interaction = .039). Conclusion: The observed association between risk of developing postmenopausal ER+ breast cancer and alcohol drinking, especially among those women who use postmenopausal hormones, may be important, because the majority of breast tumors among postmenopausal women overexpress ER.
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