| 1. |
- Koushik, Anita, et al.
(author)
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Intake of the major carotenoids and the risk of epithelial ovarian cancer in a pooled analysis of 10 cohort studies
- 2006
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In: International Journal of Cancer. - 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, Dept Med, Channing Lab, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Harvard Univ, Ctr Canc Prevent, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA. Brigham & Womens Hosp, Dept Med, Div Prevent Med, Boston, MA 02115 USA. SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY USA. TNO, Qual Life, Dept Food & Chem Risk Anal, NL-3700 AJ Zeist, Netherlands. Karolinska Inst, Natl Inst Environm Med, Div Nutrit Epidemiol, Stockholm, Sweden. NCI, Div Canc Epidemiol & Genet, NIH, Bethesda, MD 20892 USA. Amer Canc Soc, Epidemiol & Surveillance Res, Atlanta, GA 30329 USA. Univ Toronto, Fac Med, Dept Publ Hlth Sci, Toronto, ON, Canada. Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA. Maastricht Univ, NUTRIM, Dept Epidemiol, Maastricht, Netherlands. : WILEY. - 0020-7136 .- 1097-0215. ; 119:9, s. 2148-2154
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Journal article (peer-reviewed)abstract
- Carotenoids, found in fruits and vegetables, have the potential to protect against cancer because of their properties, including their functions as precursors to vitamin A and as antioxidants. We examined the associations between intakes of alpha-carotene, beta-carotene, beta-cryptoxanthin, lutein/zeaxanthin and lycopene and the risk of invasive epithelial ovarian cancer. The primary data from 10 prospective cohort studies in North America and Europe were analyzed and then pooled. Carotenoid intakes were estimated from a validated food frequency questionnaire administered at baseline in each study. Study-specific relative risks (RR) were estimated using the Cox proportional hazards model and then combined using a random-effects model. Among 521,911 women, 2,012 cases of ovarian cancer occurred during a follow-up of 7-22 years across studies. The major carotenoids were not significantly associated with the risk of ovarian cancer. The pooled multivariate RRs (95% confidence intervals) were 1.00 (0.95-1.05) for a 600 mu g/day increase in alpha-carotene intake, 0.96 (0.93-1.03) for a 2,500 mu g/day increase in beta-carotene intake, 0.99 (0.97-1.02) for a 100 mu g/day increase in beta-cryptoxanthin intake, 0.98 (0.94-1.03) for a 2,500 mu g/day increase in lutein/zeaxanthin intake and 1.01 (0.97-1.05) for a 4,000 mu g/day increase in lycopene intake. These associations did not appreciably differ by study (p-values, tests for between-studies heterogeneity > 0.17). Also, the observed associations did not vary substantially by subgroups of the population or by histological type of ovarian cancer. These results suggest that consumption of the major carotenoids during adulthood does not play a major role in the incidence of ovarian cancer. (c) 2006 Wiley-Liss, Inc.
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| 2. |
- Koushik, Anita, et al.
(author)
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Fruits, vegetables, and colon cancer risk in a pooled analysis of 14 cohort studies
- 2007
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In: Journal of the National Cancer Institute. - Univ Montreal, CHUM, Ctr Rech, Dept Social & Prevent Med, Montreal, PQ H2W 1V1, Canada. Harvard Univ, Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Biostat, Boston, MA 02115 USA. Harvard Univ, Sch Publ Hlth, Dept Epidemiol, Boston, MA 02115 USA. Loma Linda Univ, Ctr Hlth Res, Loma Linda, CA 92350 USA. Maastricht Univ, Dept Epidemiol, Maastricht, Netherlands. Amer Canc Soc, Atlanta, GA 30329 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Div Prevent Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA. Univ Buffalo State Univ New York, Dept Social & Prevent Med, Buffalo, NY 14222 USA. Roswell Pk Canc Inst, Dept Canc Prevent & Populat Sci, Buffalo, NY 14263 USA. Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA USA. TNO, Dept Food & Chem Risk Anal, Zeist, Netherlands. Univ Minnesota, Sch Publ Hlth, Div Epidemiol & Community Hlth, Minneapolis, MN USA. Wayne State Univ, Sch Med, Dept Pathol, Karmanos Canc Inst, Detroit, MI 48201 USA. Natl Canc Inst, Nutr Epidemiol Unit, I-20133 Milan, Italy. Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, Stockholm, Sweden. NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA. Univ Toronto, Fac Med, Dept Publ Hlth Sci, Toronto, ON, Canada. Natl Publ Hlth Inst, Dept Epidemiol & Hlth Promot, Helsinki, Finland. Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10467 USA. AZJ, Div Epidemiol, Dept Environm Med, New York, NY USA. : OXFORD UNIV PRESS INC. - 0027-8874 .- 1460-2105. ; 99:19, s. 1471-1483
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Journal article (peer-reviewed)abstract
- Background Fruit and vegetable intakes have been associated with a reduced risk of colon cancer; however, in more recent studies associations have been less consistent. Statistical power to examine associations by colon site has been limited in previous studies. Methods Fruit and vegetable intakes in relation to colon cancer risk were examined in the Pooling Project of Prospective Studies of Diet and Cancer. Relative risks (RRs) and 95% confidence intervals (Cis) were estimated separately in 14 studies using Cox proportional hazards model and then pooled using a randomeffects model. Intakes of total fruits and vegetables, total fruits, and total vegetables were categorized according to quintiles and absolute cutpoints. Analyses were conducted for colon cancer overall and for proximal and distal colon cancer separately. All statistical tests were two-sided. Results Among 756217 men and women followed for up to 6 to 20 years, depending on the study, 5838 were diagnosed with colon cancer. The pooled multivariable RRs (95% Cis) of colon cancer for the highest versus lowest quintiles of intake were 0.91 (0.82 to 1-01 1 P-trend =.19) for total fruits and vegetables, 0.93 (0.85 to 1.02, P-trend =.28) for total fruits, and 0.94 (0.86 to 1.02, P-trend =.17) for total vegetables. Similar results were observed when intakes were categorized by identical absolute cut points across studies (pooled multivariable FIR = 0.90, 95% CI = 0.77 to 1.05 for 800 or more versus <200 g/day of total fruits and vegetables, P-trend =.06). The age-standardized incidence rates of colon cancer for these two intake categories were 54 and 61 per 100000 person-years, respectively. When analyzed by colon site, the pooled multivariable RRs (95% Cis) comparing total fruit and vegetable intakes of 800 or more versus less than 200 g/day were 0.74 (0.57 to 0.95, P-trend =.02) for distal colon cancers and 1.02 (0.82 to 1.27, P-trend =.57) for proximal colon cancers. Similar site-specific associations were observed for total fruits and total vegetables. Conclusion Fruit and vegetable intakes were not strongly associated with colon cancer risk overall but may be associated with a lower risk of distal colon cancer.
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| 3. |
- Larsson, Susanna C., et al.
(author)
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Alcoholic beverage consumption and gastric cancer risk : A prospective population-based study in women
- 2007
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In: International Journal of Cancer. - Karolinska Inst, Div Nutr Epidemiol, Natl Inst Environm Med, 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. : WILEY. - 0020-7136 .- 1097-0215. ; 120:2, s. 373-377
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Journal article (peer-reviewed)abstract
- The association between alcohol consumption and risk of gastric cancer remains controversial. Moreover, prospective data on the role of alcoholic beverage type are sparse. We prospectively investigated the association between total alcohol (ethanol) intake as well as specific alcoholic beverages and risk of gastric cancer in the Swedish Mammography Cohort, a population-based cohort of 61,433 women. Alcohol intake and other dietary exposures were assessed at baseline (1987-1990) and again in 1997 using a food-frequency questionnaire. Incident gastric cancer cases were ascertained through the Swedish Cancer Register. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). During 966,807 person-years of follow-up, through June 2005, 160 incident cases of gastric cancer occurred. Total alcohol intake was not significantly associated with risk of gastric cancer. Compared with nondrinkers, the multivariate HR of gastric cancer for women with an alcohol intake of 40 g or more per week was 1.33 (95% CI, 0.79-2.25). Consumption of medium-strong/strong beer was associated with a statistically significant increased risk of gastric cancer; the multivariate HR for women who consumed more than one serving of medium-strong/strong beer per week (median, 2.5 drinks/week) was 2.09 (95% CI, 1.11-3.93; p-trend = 0.02) compared with no consumption. Consumption of light beer, wine, and hard liquor was not significantly associated with gastric cancer risk. Our findings suggest that constituents of beer other than alcohol may be associated with an increased risk of gastric cancer. (c) 2006 Wiley-Liss, Inc.
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| 4. |
- Larsson, Susanna C, et al.
(author)
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Association of diet with serum insulin-like growth factor I in middle-aged and elderly men
- 2005
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In: American Journal of Clinical Nutrition. - : Elsevier BV. - 0002-9165 .- 1938-3207. ; 81:5, s. 1163-7
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Journal article (peer-reviewed)abstract
- BACKGROUND: Insulin-like growth factor I (IGF-I) has been implicated in several chronic diseases, including cancer, heart disease, and osteoporosis.OBJECTIVE: Our aim was to assess whether intakes of total energy, alcohol, vitamins, minerals, and foods rich in protein and minerals (including red meat, fish and seafood, poultry, and milk) are associated with serum IGF-I concentrations in middle-aged and elderly men.DESIGN: We measured serum IGF-I concentrations in 226 free-living healthy men aged 42-76 y. The average of fourteen 24-h dietary telephone interviews performed over 1 y was used to estimate long-term dietary intake.RESULTS: We observed statistically significant positive associations between intakes of protein (P for trend = 0.001) and zinc (P for trend = 0.002) and serum IGF-I concentrations after adjusting for age. The difference in mean IGF-I concentrations for the highest compared with the lowest quintile of intake was approximately 17% (162 microg/L compared with 139 microg/L) for protein and approximately 16% (166 microg/L compared with 143 microg/L) for zinc. Consumption of red meat (P for trend = 0.05) and fish and seafood (P for trend = 0.07) was modestly positively associated with IGF-I concentrations. Other dietary factors were not associated with IGF-I concentrations.CONCLUSION: In this population of healthy well-nourished men, greater dietary intakes of protein, zinc, red meat, and fish and seafood were associated with higher IGF-I concentrations.
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| 5. |
- Larsson, Susanna C., et al.
(author)
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Body mass index and pancreatic cancer risk : A meta-analysis of prospective studies
- 2007
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In: International Journal of Cancer. - Karolinska Inst, Natl Inst Environm Med, Div Nutrit Epidemiol, S-17177 Stockholm, Sweden. : WILEY. - 0020-7136 .- 1097-0215. ; 120:9, s. 1993-1998
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Journal article (peer-reviewed)abstract
- A number of studies have examined the association between body mass index (BMI) and risk of pancreatic cancer, but uncertainty about the relationship remains. We performed a meta-analysis to summarize the evidence from prospective studies investigating this association. We searched MEDLINE for studies published in any language from 1966 to November 2006. Prospective studies were included if they reported relative risks (RRs) with 95% confidence intervals (CIs) for the association between BMI and pancreatic cancer incidence or mortality. Study-specific RR estimates were combined by use of a random-effects model. A total of 21 independent prospective studies, involving 3,495,981 individuals and 8,062 pancreatic cancer cases, met the inclusion criteria. The estimated summary RR of pancreatic cancer per 5 kg/m(2) increase in BMT was 1.12 (95% CI, 1.06-1.17; p-heterogeneity = 0.13) in men and women combined, 1.16 (95% CI, 1.05-1.28; p-heterogeneity = 0.001) in men, and 1.10 (95% CI, 1.02-1.19; p-heterogeneity = 0.12) in women. There was no evidence of publication bias (p = 0.58). Findings from this meta-analysis of prospective studies support a positive association between BMI and risk of pancreatic cancer in men and women. (c) 2007 Wilely-Liss, Inc.
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| 6. |
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| 7. |
- Larsson, Susanna C., et al.
(author)
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Carbohydrate intake, glycemic index and glycemic load in relation to risk of endometrial cancer : A prospective study of Swedish women
- 2007
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In: International Journal of Cancer. - Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden. : WILEY. - 0020-7136 .- 1097-0215. ; 120:5, s. 1103-1107
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Journal article (peer-reviewed)abstract
- The associations of carbohydrate intake, glycemic index and glycemic load with endometrial cancer risk were examined among 61,226 participants of the Swedish Mammography Cohort who were cancer-free at enrollment between 1987 and 1990 and completed a food frequency questionnaire. During a mean follow-up of 15.6 years, through June 2005, 608 incident cases of endometrial adenocarcinoma were diagnosed. We observed no overall association between carbohydrate intake, glycemic index or glycemic load and incidence of endometrial cancer; the rate ratios (RRs) for the highest versus the lowest quintile were 1.12 (95% CI, 0.85-1.47) for carbohydrate intake, 1.00 (95% CI, 0.77-1.30) for glycemic index and 1.15 (95% CI, 0.88-1.51) for glycemic load. However, among obese women (body mass index, BMI >= 30 kg/m(2)), endometrial cancer incidence was nonsignificantly elevated in the top versus bottom quintiles of carbohydrate intake (RR, 1.68; 95% CI, 0.86-3.29) and glycemic load (RR, 1.57; 95% CI, 0.82-2.99). In a subanalysis of women who completed a follow-up questionnaire in 1997, which collected information on physical activity, carbohydrate intake and glycemic load were positively related to endometrial cancer risk among overweight women (BMI >= 25 kg/m(2)) with low physical activity. In this subgroup, the multivariate RRs comparing extreme quartiles were 1.90 (95% CI, 0.84-4.31) for carbohydrate intake and 2.99 (95% CI, 1.17-7.67) for glycemic load. Results from this cohort study suggest that a high carbohydrate intake and a high glycemic load may increase the risk of endometrial cancer among overweight women with low physical activity. (c) 2006 Wiley-Liss, Inc.
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| 8. |
- Larsson, Susanna C., et al.
(author)
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Coffee and black tea consumption and risk of breast cancer by estrogen and progesterone receptor status in a Swedish cohort
- 2009
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In: Cancer Causes and Control. - : Springer Science and Business Media LLC. - 0957-5243 .- 1573-7225. ; 20:10, s. 2039-2044
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Journal article (peer-reviewed)abstract
- Coffee and tea consumption has been inconsistently associated with the risk of breast cancer. We examined the associations of caffeinated coffee and black tea consumption with the incidence of breast cancer, overall and by estrogen receptor (ER) and progesterone receptor (PR) status of the tumor, in the Swedish Mammography Cohort. We prospectively followed up 61,433 women who were cancer free at baseline in 1987-1990. Coffee and tea consumption was assessed with a food-frequency questionnaire administered at baseline and in 1997. Incident invasive breast cancer cases were ascertained by linkage with Swedish Cancer registers. Over a mean follow-up of 17.4 years, through December 2007, there were 2,952 incident cases of invasive breast cancer identified. Coffee consumption was not associated with risk of overall breast cancer (multivariate relative risk (RR) for a parts per thousand yen4 cups/day versus < 1 cup/day = 1.02; 95% CI, 0.87-1.20) or with any subtype defined by ER and PR status. Black tea consumption was significantly positively associated with risk of overall breast cancer and ER+/PR+ tumors. The multivariate RRs comparing a parts per thousand yen2 cups/day of tea with no consumption were 1.22 (95% CI, 1.05-1.42) for overall breast cancer and 1.36 (95% CI, 1.09-1.69) for ER+/PR+ tumors. Findings from this prospective study do not support a role of coffee consumption in the development of breast cancer but suggest that black tea consumption may be positively associated with risk of ER+/PR+ tumors.
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| 9. |
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| 10. |
- Larsson, Susanna C., et al.
(author)
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Coffee consumption and stomach cancer risk in a cohort of Swedish women
- 2006
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In: International Journal of Cancer. - Karolinska Inst, Natl Inst Environm Med, Div Nutrit Epidemiol, SE-17177 Stockholm, Sweden. Harvard Univ, Sch Publ Hlth, Dept Nutr & Epidemiol, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. : WILEY-LISS. - 0020-7136 .- 1097-0215. ; 119:9, s. 2186-2189
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Journal article (peer-reviewed)abstract
- Few prospective studies have examined the relationship between coffee consumption and risk of stomach cancer, and the findings have been inconsistent. We prospectively investigated the association of long-term coffee consumption with risk of stomach cancer in a population-based cohort study of 61,433 Swedish women. Information on coffee consumption was collected with a food-frequency questionnaire at baseline (1987-1990) and updated in 1997. During a mean follow-up of 15.7 years from 1987 through June 2005, 160 incident cases of stomach cancer were diagnosed. Coffee consumption was positively associated with the risk of stomach cancer. Compared to women who consumed I or fewer cups of coffee per day, the multivariate hazard ratios were 1.49 (95% = 0.97-2.27) for women who drank 2-3 cups per day and 1.86 (95% CI = 1.07-3.25) for those who drank 4 or more cups per day (p for trend = 0.01). An increase of 1 cup of coffee per day was associated with a statistically significant 22% increased risk of stomach cancer (hazard ratio = 1.22; 95% CI = 1.051.42). These prospective data suggest that coffee consumption may increase the risk of stomach cancer in a dose-response manner. This finding needs to be confirmed in other prospective studies. (c) 2006 Wiley-Liss, Inc.
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