| 51. |
- Friberg, Emilie, et al.
(författare)
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Diabetes and risk of endometrial cancer : A population-based prospective cohort study
- 2007
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Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - Karolinska Inst, Div Nutr Epidemiol, Natl Inst Environm Med, SE-17177 Stockholm, Sweden. Harvard Univ, Beth Israel Deaconess Med Ctr, Sch Med, Div Endocrinol Diabet & Metab,Dept Med, Boston, MA 02215 USA. : AMER ASSOC CANCER RESEARCH. - 1055-9965 .- 1538-7755. ; 16:2, s. 276-280
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Tidskriftsartikel (refereegranskat)abstract
- Although there is accumulating evidence that hyperinsulinemia in the context of insulin resistance is associated with carcinogenesis, only one prospective study of endometrial cancer incidence, in relation to diabetes, addressed this issue and showed no significant positive association. No previous study has investigated whether physical activity can modify the association between diabetes and endometrial cancer. We examined the association between diabetes and incidence of endometrial cancer and the potential effect modification by obesity and physical activity in the Swedish Mammography Cohort, a prospective cohort of 36,773 women, including 225 incident endometrial adenocarcinoma cases. After adjustments, the relative risk (RR) for endometrial cancer among women with diabetes comparing with nondiabetic women was 1.94 [95% confidence interval (95% CI), 1.23-3.08]. Among obese diabetics, the RR was 6.39 (95% CI, 3.28-12.06) compared with nonobese nondiabetic women. Among diabetics with low physical activity, the RR for endometrial cancer was 2.80 (95% CI, 1.62-4.85) compared with physically active nondiabetic women. Obese diabetics with low physical activity had a RR of 9.61 (95% CI, 4.66-19.83) compared with normal weight nondiabetic women with high physical activity. Diabetes was associated with a 2-fold increased risk, and combination of diabetes with obesity and low physical activity was associated with a further increased risk for endometrial cancer. Interventions to reduce body weight and increase physical activity may have important implications in terms of prevention of endometrial cancer and future management of diabetic subjects.
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| 52. |
- Friberg, Emilie, et al.
(författare)
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Long-term Alcohol Consumption and Risk of Endometrial Cancer Incidence : A Prospective Cohort Study
- 2009
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Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - : AMER ASSOC CANCER RESEARCH. - 1055-9965 .- 1538-7755. ; 18:1, s. 355-358
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Tidskriftsartikel (refereegranskat)abstract
- Alcohol consumption has been hypothesized to increase the risk of endometrial cancer. We used data from the prospective population-based Swedish Mammography Cohort including 61,226 women to examine the association between alcohol and endometrial cancer incidence. Alcohol consumption was assessed with validated food frequency questionnaires at baseline 1.987 to 1.990 and at follow-up in 1997. During a mean follow-up of 17.6 years, 687 endometrial cancer cases were identified in the Swedish cancer registries. We found no association between alcohol consumption and endometrial cancer risk after adjustment for age, body mass index, and smoking, The multivariable rate ratios (95% confidence intervals) for the three upper categories of long-term alcohol consumption as compared with no consumption were 1.01 (0.84-1.22) for <3.4 g/d, 1.01 (0.80-1.27) for 3.4 to 9.9 g/d, and 1.09 (0.71-1.67) for >= 1.0 g/d, respectively. The association did not differ by age, body mass index, folic acid intake, or postmenopausal hormone use in stratified analysis. In conclusion, our results suggest that low alcohol consumption (up to one drink per day) is unlikely to substantially influence risk of endometrial cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(1):355-8)
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| 53. |
- Friberg, Emilie, et al.
(författare)
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Physical activity and risk of endometrial cancer : A population-based prospective cohort study
- 2006
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Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - Karolinska Inst, Div Nutr Epidemiol, Natl Inst Environm Med, SE-17177 Stockholm, Sweden. Harvard Univ, Sch Med, Div Endocrinol Diabet & Metab, Dept Med,Beth Israel Deaconess Med Ctr, Boston, MA 02115 USA. : AMER ASSOC CANCER RESEARCH. - 1055-9965 .- 1538-7755. ; 15:11, s. 2136-2140
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Tidskriftsartikel (refereegranskat)abstract
- Physical activity is involved in the regulation of metabolic and hormonal pathways and is one of the factors important for the maintenance of body weight; obesity is a risk factor for endometrial cancer. A connection between physical activity and endometrial cancer risk through hormonal mechanisms, possibly mediated by body weight, is biologically plausible. Only one study has investigated total physical activity, and no previous study has examined leisure time inactivity directly. We investigated the association of total physical activity and different types of physical activity with risk of endometrial cancer in the Swedish Mammography Cohort, a population-based prospective cohort, including 33,723 women and 199 endometrial cancer cases. After adjustments for potential confounders (age, body mass index, parity, history of diabetes, total fruit and vegetable intake, and education), the relative risks for endometrial cancer for the second to fourth quartile of total physical activity compared with the lowest one were 0.80 [95% confidence interval (95% CI), 0.54-1.18], 0.87 (95% CI, 0.59-1.28), and 0.79 (95% CI, 0.53-1.17). High leisure time inactivity (watching TV/sitting >= 5 hours daily) compared with low was associated with increased risk of endometrial cancer (relative risk, 1.66; 95% CI, 1.05-2.61). The associations were not modified by body mass index. Findings from this study suggest that total physical activity is weakly inversely associated with endometrial cancer risk and that leisure time inactivity is statistically significantly associated with increased risk for endometrial cancer.
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| 54. |
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| 55. |
- 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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| 56. |
- Genkinger, J M, et al.
(författare)
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Dairy products and ovarian cancer : A pooled analysis of 12 cohort studies
- 2006
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Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - 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. Brigham & Womens Hosp, Channing Lab, Boston, MA 02115 USA. Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA. Brigham & Womens Hosp, Div Prevent Med, Boston, MA 02115 USA. Harvard Univ, Sch Med, Boston, MA USA. Univ Minnesota, Sch Publ Hlth, Div Epidemiol, Minneapolis, MN 55455 USA. NYU, Dept Environm Med, Div Epidemiol, New York, NY 10016 USA. Loma Linda Univ, Sch Med, Ctr Hlth Res, Loma Linda, CA USA. SUNY Buffalo, Dept Social & Prevent Med, Buffalo, NY 14260 USA. Netherlands Org Appl Sci Res Qual Life, Dept Food & Chem Risk Anal, Zeist, Netherlands. Univ Oslo, Dept Nutr, Oslo, Norway. NCI, Div Canc Epidemiol & Genet, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. Natl Inst Environm Med, Div Nutr Epidemiol, Karolinska Inst, Stockholm, Sweden. Amer Canc Soc, 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, Dept Epidemiol, Nutr & Toxicol Res Inst, Maastricht, Netherlands. : AMER ASSOC CANCER RESEARCH. - 1055-9965 .- 1538-7755. ; 15:2, s. 364-372
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Tidskriftsartikel (refereegranskat)abstract
- Background: Dairy foods and their constituents (lactose and calcium) have been hypothesized to promote ovarian carcinogenesis. Although case-control studies have reported conflicting results for dairy foods and lactose, several cohort studies have shown positive associations between skim milk, lactose, and ovarian cancer. Methods: A pooled analysis of the primary data from 12 prospective cohort studies was conducted. The study population consisted of 553,217 women among whom 2,132 epithelial ovarian cases were identified. Study-specific relative risks and 95% confidence intervals were calculated by Cox proportional hazards models and then pooled by a random-effects model. Results: No statistically significant associations were observed between intakes of milk, cheese, yogurt, ice cream, and dietary and total calcium intake and risk of ovarian cancer. Higher lactose intakes comparing >= 30 versus < 10 g/d were associated with a statistically significant higher risk of ovarian cancer, although the trend was not statistically significant (pooled multivariate relative risk, 1.19; 95% confidence interval, 1.01-1.40; P-trend = 0.19). Associations for endometrioid, mucinous, and serous ovarian cancer were similar to the overall findings. Discussion: Overall, no associations were observed for intakes of specific dairy foods or calcium and ovarian cancer risk. A modest elevation in the risk of ovarian cancer was seen for lactose intake at the level that was equivalent to three or more servings of milk per day. Because a new dietary guideline recommends two to three servings of dairy products per day, the relation between dairy product consumption and ovarian cancer risk at these consumption levels deserves further examination.
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| 57. |
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| 58. |
- Goodman, Anna, et al.
(författare)
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Maternal pelvic size not predictive of daughter's breast cancer or ovarian cancer in a large Swedish cohort
- 2009
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Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - 1055-9965 .- 1538-7755. ; 18:8, s. 2333-2335
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Tidskriftsartikel (refereegranskat)abstract
- Recent studies from Finland reported that maternal pelvic size predicted daughters' breast and ovarian cancer, possibly because maternal pelvic size is a marker for in utero hormone exposure. We sought to replicate this association in 3,845 women born between 1915 and 1929 in Uppsala, Sweden, and followed from 1960 to 2002. Archived obstetric records provided the standard measures of maternal pelvic size (intercristal distance, interspinous distance, the intercristal-interspinous difference, and the external conjugate distance). The Swedish Cancer Registry ascertained cancer incidence, with 273 cohort members developing primary breast cancer, and 52 developing primary ovarian cancer during the follow-up period. There was no evidence (P > 0.1) of an association between any measure of maternal pelvic size and incidence of either breast or ovarian cancer. This was true both before and after adjustment for various characteristics of the women and their mothers, and in analyses stratified by age at diagnosis (<50 versus ≥50 years of age, as a proxy for premenopausal and postmenopausal ages). There was also no evidence of an association in subgroup analyses restricted specifically to those groups in which the Finnish data found the greatest effect. Our study is of comparable size to the Finnish studies and was highly powered (>99%) to detect effects of the magnitude they reported. Our nonreplication therefore casts doubt on the link between maternal pelvic size and risk of breast and ovarian cancer in the offspring. (Cancer Epidemiol Biomarkers
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| 59. |
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| 60. |
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