| 1. |
- Genkinger, Jeanine M., et al.
(författare)
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Alcohol Intake and Pancreatic Cancer Risk : A Pooled Analysis of Fourteen Cohort Studies
- 2009
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Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - 1055-9965 .- 1538-7755. ; 18:3, s. 765-776
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Forskningsöversikt (refereegranskat)abstract
- Background: Few risk factors have been implicated in pancreatic cancer etiology. Alcohol has been theorized to promote carcinogenesis. However, epidemiologic studies have reported inconsistent results relating alcohol intake to pancreatic cancer risk. Methods: We conducted a pooled analysis of the primary data from 14 prospective cohort studies. The study sample consisted of 862,664 individuals among whom 2,187 incident pancreatic cancer cases were identified. Study-specific relative risks and 95% confidence intervals were calculated using Cox proportional hazards models and then pooled using a random effects model. Results: A slight positive association with pancreatic cancer risk was observed for alcohol intake (pooled multivariate relative risk, 1.22; 95% confidence interval, 1.03-1.45 comparing >= 30 to 0 grams/day of alcohol; P value, test for between-studies heterogeneity = 0.80). For this comparison, the positive association was only statistically significant among women although the difference in the results by gender was not statistically significant (P value, test for interaction = 0.19). Slightly stronger results for alcohol intake were observed when we limited the analysis to cases with adenocarcinomas of the pancreas. No statistically significant associations were observed for alcohol from wine, beer, and spirits comparing intakes of >= 5 to 0 grams/day. A stronger positive association between alcohol consumption and pancreatic cancer risk was observed among normal weight individuals compared with overweight and obese individuals (P value, test for interaction = 0.01). Discussion: Our findings are consistent with a modest increase in risk of pancreatic cancer with consumption of 30 or more grams of alcohol per day. (Cancer Epidemiol Biomarkers Prev 2009;18(3):765-76)
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| 2. |
- Koushik, Anita, et al.
(författare)
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Fruits, vegetables, and colon cancer risk in a pooled analysis of 14 cohort studies
- 2007
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Ingår i: 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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Tidskriftsartikel (refereegranskat)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.
(författare)
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Alcoholic beverage consumption and gastric cancer risk : A prospective population-based study in women
- 2007
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Ingår i: 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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Tidskriftsartikel (refereegranskat)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. |
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| 5. |
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| 6. |
- Larsson, Susanna C., et al.
(författare)
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Coffee consumption and stomach cancer risk in a cohort of Swedish women
- 2006
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Ingår i: 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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Tidskriftsartikel (refereegranskat)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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| 7. |
- Larsson, Susanna C., et al.
(författare)
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Dietary carbohydrate, glycemic index, and glycemic load in relation to risk of colorectal cancer in women
- 2007
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Ingår i: American Journal of Epidemiology. - 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, Dept Med, Channing Lab, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. : OXFORD UNIV PRESS INC. - 0002-9262 .- 1476-6256. ; 165:3, s. 256-261
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Tidskriftsartikel (refereegranskat)abstract
- Diets with a high glycemic index and glycemic load have been hypothesized to be implicated in the etiology of colorectal cancer owing to their potential to increase postprandial glucose and insulin levels. Prospective data on glycemic index and glycemic load in relation to colorectal cancer risk are limited and inconsistent. Therefore, the authors prospectively investigated the associations of dietary carbohydrate, glycemic index, and glycemic load with the incidence of colorectal cancer among 61,433 Swedish women who were free of cancer in 1987-1990 and completed a 67-item food frequency questionnaire. During follow-up through June 2005, 870 incident cases of colorectal adenocarcinoma were diagnosed. Carbohydrate intake, glycemic index, and glycemic load were not associated with risk of colorectal cancer, colon cancer, or rectal cancer. The multivariate hazard ratios for colorectal cancer comparing the highest with the lowest quintile were 1.10 (95% confidence interval: 0.85, 1.44) for carbohydrate intake, 1.00 ( 95% confidence interval: 0.75, 1.33) for glycemic index, and 1.06 ( 95% confidence interval: 0.81, 1.39) for glycemic load. Results did not vary by body mass index. The findings from this prospective study do not support the hypothesis that a high carbohydrate intake, a high glycemic index, and a high glycemic load increase the risk of colorectal cancer.
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| 8. |
- Larsson, Susanna C., et al.
(författare)
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Folate intake and stomach cancer incidence in a prospective cohort of Swedish women
- 2006
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Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - Natl Inst Environm Med, Karolinska Inst, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden. Harvard Sch Publ Hlth, Dept Nutr, Boston, MA USA. Harvard Sch Publ Hlth, Dept Epidemiol, Boston, MA USA. Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA. Harvard Univ, Sch Med, Boston, MA USA. : AMER ASSOC CANCER RESEARCH. - 1055-9965 .- 1538-7755. ; 15:7, s. 1409-1412
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Tidskriftsartikel (refereegranskat)abstract
- Background: Experimental and epidemiologic evidence suggests that folate may play a role in the development of some cancers. Case-control studies and one prospective cohort study on folate intake in relation to stomach cancer risk have yielded inconsistent results. Methods: We prospectively investigated the relation between folate intake and the incidence of stomach cancer among 61,433 women in the Swedish Mammography Cohort. Participants completed a food frequency questionnaire at baseline (1987-1990) and again in 1997. During follow-up through December 2004, 156 incident stomach cancer cases were diagnosed. Cox proportional hazards models were used to calculate multivariate-adjusted hazard ratios. Results: There was no association between dietary folate intake (i.e., folate from food sources) and the risk of stomach cancer. The multivariate hazard ratio for the highest compared with the lowest category of updated average dietary folate intake was 1.04 (95% confidence interval, 0.61-1.86; P-trend = 0.91). The relation between dietary folate intake and stomach cancer did not vary significantly by intake of alcohol, methionine, or caffeine. Conclusion: Results from this prospective study do not support an association between dietary folate intake and risk of stomach cancer.
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| 9. |
- Larsson, Susanna C., et al.
(författare)
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Folate intake, MTHFR polymorphisms, and risk of esophageal, gastric, and pancreatic cancer : A meta-analysis
- 2006
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Ingår i: Gastroenterology. - Karolinska Inst, Natl Inst Environm Med, Div Nutr Epidemiol, SE-17177 Stockholm, Sweden. Harvard Univ, Sch Med, 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. Brigham & Womens Hosp, Dept Med, Channing Lab, Boston, MA USA. : W B SAUNDERS CO-ELSEVIER INC. - 0016-5085 .- 1528-0012. ; 131:4, s. 1271-1283
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Tidskriftsartikel (refereegranskat)abstract
- Background & Aims: Increasing evidence suggests that a low folare intake and impaired folate metabolism may be implicated in the development of gastrointestinal cancers. We conducted a systematic review with meta-analysis of epidemiologic studies evaluating the association of folate intake or genetic polymorphisms in S,10-methylenetetrahydrofolate reductase (MTHFR), a central enzyme in folate metabolism, with risk of esophageal, gastric, or pancreatic cancer. Methods: A literature search was performed using MEDLINE for studies published through March 2006. Study-specific relative risks were weighted by the inverse of their variance to obtain random-effects summary estimates. Results: The summary relative risks for the highest versus the lowest category of dietary folate intake were 0.66 (9S% confidence interval [CI], 0.53-0.83) for esophageal squamous cell carcinoma (4 case-control), 0.50 (9S% CI, 0.39-0.65) for esophageal adenocarcinoma (3 casecontrol), and 0.49 (95% CI, 0.3S-0.67) for pancreatic cancer (I case-control, 4 cohort); there was no heterogeneity among studies. Results on dietary folate intake and risk of gastric cancer (9 case-control, 2 cohort) were inconsistent. In most studies, the MTHFR 677TT (variant) genotype, which is associated with reduced enzyme activity, was associated with an increased risk of esophageal squamous cell carcinoma, gastric cardia adenocarcinoma, noncardia gastric cancer, gastric cancer (all subsites), and pancreatic cancer; all but one of 22 odds ratios were > 1, of which 13 estimates were statistically significant. Studies of the MTHFR A1298C polymorphism were limited and inconsistent. Conclusions: These findings support the hypothesis that folare may play a role in carcinogenesis of the esophagus, stomach, and pancreas.
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| 10. |
- Larsson, Susanna G., et al.
(författare)
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Methionine and vitamin B-6 intake and risk of pancreatic cancer : A prospective study of Swedish women and men
- 2007
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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. Brigham & Womens Hosp, Channing Lab, Dept Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. : W B SAUNDERS CO-ELSEVIER INC. - 0016-5085 .- 1528-0012. ; 132:1, s. 113-118
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Tidskriftsartikel (refereegranskat)abstract
- Background & Aims: It has been hypothesized that dietary factors involved in methyl group metabolism, such as methionine, folate, and vitamin B-6, may modify cancer risk. We have previously reported an inverse association between folate intake and pancreatic cancer risk in a prospective population-based cohort of Swedish women and men. In the present study, we used data from this prospective study to examine whether methionine and vitamin B6 intakes were associated with the incidence of exocrine pancreatic cancer. Methods: Our study population comprised 81,922 Swedish women and men, aged 45-83 years, who were free from cancer and completed a self-administered food-frequency questionnaire in 1997. We used Cox proportional hazards models to estimate rate ratios with 95% confidence intervals (CI), adjusted for age, sex, education, smoking, body mass index, diabetes, and intakes of total energy and dietary folate. Results: During a mean follow-up of 7.2 years, through June 2005, 147 incident cases of pancreatic cancer were diagnosed. Methionine intake was significantly inversely associated with risk of pancreatic cancer, whereas no significant association was observed for dietary or total vitamin B6 intake. The multivariate rate ratios comparing the highest with the lowest quartile of methionine intake were 0.44 (95% CI, 0.26-0.73; P for trend = .0005) in women and men combined, 0.59 (95% CI, 0.28-1.21; P for trend = .07) in women, and 0.32 (95% CI, 0.15-0.65; P for trend = .002) in men. Conclusions: These findings suggest that higher methionine intake may reduce the risk of pancreatic cancer.
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