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  • COHORT  (7)
  • RELATIVE RISK  (7)
  • 1
    Keywords: CANCER ; Germany ; LUNG ; FOLLOW-UP ; INFORMATION ; lung cancer ; LUNG-CANCER ; COHORT ; cohort study ; EPIDEMIOLOGY ; EXPOSURE ; MORTALITY ; occupation ; POPULATION ; RISK ; RISKS ; REDUCTION ; RISK-FACTORS ; ASSOCIATION ; HUMANS ; WOMEN ; MEN ; risk factors ; smoking ; COUNTRIES ; cancer risk ; POPULATIONS ; DIET ; VALIDITY ; EPIC ; nutrition ; SMOKERS ; RELATIVE RISK ; exercise ; physical activity ; REGRESSION ; ASSOCIATIONS ; PHYSICAL-ACTIVITY ; INTERVAL ; SUBTYPES ; prospective ; UNIT ; RISK-FACTOR ; CANCER-RISK ; sports ; occupations ; ACTIVITY QUESTIONNAIRE
    Abstract: Research conducted predominantly in male populations on physical activity and lung cancer has yielded inconsistent results. We examined this relationship among 416,277 men and women from the European Prospective Investigation into Cancer and Nutrition (EPIC). Detailed information on recent recreational, household and occupational physical activity, smoking habits and diet was assessed at baseline between 1992 and 2000. Relative risks (RR) were estimated using Cox regression. During 6.3 years of follow-up we identified 607 men and 476 women with incident lung cancer. We did not observe an inverse association between recent occupational, recreational or household physical activity and lung cancer risk in either males or females. However, we found some reduction in lung cancer risk associated with sports in males (adjusted RR = 0.71; 95% confidence interval 0.50-0.98; highest tertile vs. inactive group), cycling (RR = 0.73; 0.54-0.99) in females and non-occupational vigorous physical activity. For occupational physical activity, lung cancer risk was increased for unemployed men (adjusted RR = 1.57; 1.20-2.05) and men with standing occupations (RR = 1.35; 1.02-1.79) compared with sitting professions. There was no evidence of heterogeneity of physical activity associations across countries, or across any of the considered cofactors. For some histologic subtypes suggestive sex-specific reductions, limited by subgroup sizes, were observed, especially with vigorous physical activity. In total, our study shows no consistent protective associations of physical activity with lung cancer risk. It can be assumed that the elevated risks found for occupational physical activity are not produced mechanistically by physical activity itself but rather reflect exposure to occupation-related lung cancer risk factors. (c) 2006 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16894558
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  • 2
    Keywords: CANCER ; MODEL ; MODELS ; FOLLOW-UP ; RISK ; METABOLISM ; INDEX ; CARCINOGENESIS ; ASSOCIATION ; BREAST-CANCER ; NO ; hormone ; PLASMA ; NUMBER ; WOMEN ; OBESITY ; cancer risk ; ORAL-CONTRACEPTIVES ; cholesterol ; LIPOPROTEIN ; LOW-DENSITY-LIPOPROTEIN ; case-control studies ; ABNORMALITIES ; BODY ; DIABETES-MELLITUS ; EPIC ; European Prospective Investigation into Cancer and Nutrition ; nutrition ; ENDOMETRIAL CANCER ; RELATIVE RISK ; REGRESSION-MODELS ; CLUSTER ; POSTMENOPAUSAL WOMEN ; MASS INDEX ; MASSES ; BODIES ; ONCOLOGY ; case control study ; case-control study ; REGRESSION ; ASSOCIATIONS ; ENDOMETRIAL ; RE ; INCREASE ; BODY-SIZE ; PHYSICAL-ACTIVITY ; LEVEL ; case control studies ; INTERVAL ; metabolic syndrome ; HORMONES ; prospective ; UNIT ; CANCER-RISK ; C-PEPTIDE ; SET ; case control ; LOGISTIC-REGRESSION ; BODY-MASS ; BODY-MASS-INDEX ; lipid ; HDL-CHOLESTEROL ; LOW-DENSITY ; SERUM-CHOLESTEROL
    Abstract: To clarify the role of metabolic factors in endometrial carcinogenesis, we conducted a case-control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC), and examined the relation between prediagnostic plasma lipids, lipoproteins, and glucose, the metabolic syndrome (MetS; a cluster of metabolic factors) and endometrial cancer risk. Among pre- and postmenopausal women, 284 women developed endometrial cancer during follow-up. Using risk set sampling, 546 matched control subjects were selected. From conditional logistic regression models, high-density lipoprotein cholesterol (HDL-C) levels were inversely associated with risk body mass index (BMI)-adjusted relative risk (FR) for top versus bottom quartile 0.61 (95% confidence intervals (CI) 0.38-0.97), P-trend= 0.02). Glucose levels were positively associated with risk (BMI-adjusted RR top versus bottom quartile 1.69 (95% Cl 0.99-2.90), P-trend, = 0.03), which appeared stronger among postmenopausal women (BMI-adjusted RR top versus bottom tertile 2.61 (95% Cl 1.46-4.66), P-trend=0.0006, P-heterogeneity=0.13) and never-users of exogenous hormones (P-heterogeneity=0-005 for oral contraceptive (OC) use and 0.05 for hormone replacement therapy-use). The associations of HDL-C and glucose with risk were no longer statistically significant after further adjustment for obesity-related hormones. Plasma total cholesterol, Low-density lipoprotein cholesterol (LDL-C), and triglycerides were not significantly related to overall risk. The presence of MetS was associated with risk (RR 2.12 (95% CI 1.51-2.97)), which increased with the number of MetS factors (P-trend=0.02). An increasing number of MetS factors other than waist circumference, however, was marginally significantly associated with risk only in women with waist circumference above the median (P-interaction=0-01). None of the associations differed significantly by fasting status. These findings suggest that metabolic abnormalities and obesity may act synergistically to increase endometrial cancer risk
    Type of Publication: Journal article published
    PubMed ID: 17914105
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  • 3
    Keywords: CANCER ; MODEL ; MODELS ; THERAPY ; FOLLOW-UP ; COHORT ; cohort studies ; EXPOSURE ; RISK ; RISKS ; INDEX ; ASSOCIATION ; NO ; hormone ; HEALTH ; WOMEN ; HORMONE REPLACEMENT THERAPY ; cancer risk ; FIBER ; MEASUREMENT ERROR ; DIET ; DIETARY ; FAT ; European Prospective Investigation into Cancer and Nutrition ; nutrition ; AUSTRALIA ; ENDOMETRIAL CANCER ; RELATIVE RISK ; dietary fiber ; insulin ; IGF-I ; ASSOCIATIONS ; ENDOMETRIAL ; THERAPIES ; ENERGY-INTAKE ; PHYSICAL-ACTIVITY ; LEVEL ; INTERVAL ; USA ; prospective ; INSULIN SENSITIVITY ; VARIABLES ; CANCER-RISK ; C-PEPTIDE ; FOODS ; Nutrition Assessment ; postmenopausal ; DIANA RANDOMIZED-TRIAL ; dietary carbohydrates ; endometrial neoplasms ; glycemic index ; IOWA WOMENS HEALTH
    Abstract: The associations of dietary total carbohydrates, overall glycemic index, total dietary glycemic load, total sugars, total starch, and total fiber with endometrial cancer risk were analyzed among 288,428 women in the European Prospective Investigation into Cancer and Nutrition cohort (1992-2004), including 710 incident cases diagnosed during a mean 6.4 years of follow-up. Cox proportional hazards models were used to estimate relative risks and 95% confidence intervals. There were no statistically significant associations with endometrial cancer risk for increasing quartile intakes of any of the exposure variables. However, in continuous models calibrated by using 24-hour recall values, the multivariable relative risks were 1.61 (95% confidence interval: 1.06, 2.45) per 100 g/day of total carbohydrates, 1.40 (95% confidence interval: 0.99, 1.99) per 50 units/day of total dietary glycemic load, and 1.36 (95% confidence interval: 1.05, 1.76) per 50 g/day of total sugars. These associations were stronger among women who had never used postmenopausal hormone therapy compared with ever users (total carbohydrates P-heterogeneity = 0.04). Data suggest no association of overall glycemic index, total starch, and total fiber with risk, and a possible modest positive association of total carbohydrates, total dietary glycemic load, and total sugars with risk, particularly among never users of hormone replacement therapy
    Type of Publication: Journal article published
    PubMed ID: 17670911
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  • 4
    Keywords: CANCER ; DIAGNOSIS ; COHORT ; RISK ; ASSOCIATION ; breast cancer ; BREAST-CANCER ; WOMEN ; OBESITY ; SWEDEN ; POSTMENOPAUSAL WOMEN ; leptin ; IGF-I ; case-control study ; WEIGHT ; GROWTH-FACTOR-I ; OVERWEIGHT ; prospective ; C-PEPTIDE ; SERUM ADIPONECTIN ; Adiponectin ; NORTHERN SWEDEN ; GLUCOSE-HOMEOSTASIS ; Glycated haemoglobin
    Abstract: It is hypothesized that insulin resistance and related metabolic factors may influence breast cancer risk, however the epidemiological evidence remains inconclusive. We conducted a case-control study nested in a prospective cohort in Northern Sweden, to clarify the associations of body mass index (BMI), leptin, adiponectin, C-peptide, and glycated haemoglobin (HbA1c) with breast cancer risk. We also investigated whether these associations may be modified by age at diagnosis, tumour stage, and oestrogen and progesterone receptor status. During follow-up, 561 women developed invasive breast cancer and 561 matched controls were selected. Conditional logistic regression was used to calculate odds ratios (OR) as estimates of relative risk, and 95% confidence intervals (CI). The associations of BMI, leptin and HbA1c with breast cancer risk differed significantly according to whether the tumour was diagnosed as stage I or stage II-IV (P (heterogeneity) all 〈 0.05). These factors were significantly inversely associated with risk in the group of stage I tumours, with ORs for top vs. bottom tertile for BMI of 0.48 (95% CI, 0.30-0.78, P (trend) = 0.004); leptin, 0.64 (95% CI, 0.41-1.00, P (trend) = 0.06); and HbA1c, 0.47 (95% CI, 0.28-0.80, P (trend) = 0.005). For stage II-IV tumours, there was a suggestion of an increased risk with higher levels of these factors. There were no significant differences in the associations of BMI, leptin, adiponectin, C-peptide and HbA1c with breast cancer risk in subgroups of age at diagnosis or tumour receptor status. This prospective study suggests that BMI, leptin and HbA1c influence breast tumour initiation and progression
    Type of Publication: Journal article published
    PubMed ID: 18330696
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  • 5
    Keywords: CANCER ; Germany ; FOLLOW-UP ; INFORMATION ; COHORT ; EPIDEMIOLOGY ; EXPOSURE ; RISK ; TIME ; REDUCTION ; RISK-FACTORS ; NO ; HEALTH ; WOMEN ; CIGARETTE-SMOKING ; PROSPECTIVE COHORT ; risk factors ; smoking ; cancer risk ; RECRUITMENT ; EPIC ; European Prospective Investigation into Cancer and Nutrition ; nutrition ; ENDOMETRIAL CANCER ; HETEROGENEITY ; POSTMENOPAUSAL WOMEN ; IGF-I ; ONCOLOGY ; ENDOMETRIAL ; RE ; WEIGHT ; prospective studies ; PHYSICAL-ACTIVITY ; EPIDEMIOLOGIC EVIDENCE ; PREMENOPAUSAL WOMEN ; sex-steroid hormones ; USA ; REPLACEMENT THERAPY ; PREMENOPAUSAL ; prospective ; prospective study ; INCREASED RISK ; NEVER SMOKERS ; RISK-FACTOR ; CANCER-RISK ; HEALTHY WOMEN ; postmenopausal
    Abstract: Current epidemiologic evidence indicates that cigarette smoking reduces the risk of endometrial cancer. We examined data from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort to analyze further aspects of the smoking-endometrial cancer relationship, such as possible modifying effects of menopausal status, HRT use, BMI and parity. In a total of 249,986 women with smoking exposure and menopausal status information, 619 incident endometrial cancer cases were identified during 1.56 million person-years of follow-up. Among postmenopausal women, the hazard ratio (HR) for current smokers versus never smokers was 0.70 (95% CI = 0.53-0.93), while it was 1.75 (95% CI = 1.13-2.70) among premenopausal women at recruitment. After adjustment for risk factors, the HR for postmenopausal women was slightly attenuated to 0.78 (95% CI = 0.59-1.03). No heterogeneity of effect was observed with HRT use or BMI. Among premenopausal women, current smokers of more than 15 cigarettes per day or who smoked for 30 years or more at the time of recruitment had a more than 2-fold increased risk of endometrial cancer compared to never smokers (HR = 2.54; 95% CI = 1.47-4.38 and HR = 2.23; 95% CI = 1.04-4.77, respectively). Past smoking was not associated with endometrial cancer risk, either among pre- or post-menopausal women. In this prospective study, we observed an increased risk of endometrial cancer with cigarette smoking in premenopausal women. The reduction of endometrial cancer risk observed among postmenopausal women does not have direct public health relevance since cigarette smoking is the main known risk factor for cancer. (c) 2007 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17657712
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  • 6
    Keywords: APOPTOSIS ; CANCER ; proliferation ; BLOOD ; CELL ; CELL-PROLIFERATION ; Germany ; MODEL ; MODELS ; COHORT ; RISK ; RISKS ; SITE ; PROTEIN ; PROTEINS ; colon ; BINDING ; ASSOCIATION ; NO ; resistance ; NUMBER ; AGE ; WOMEN ; colorectal cancer ; OBESITY ; COLORECTAL-CANCER ; COUNTRIES ; RATES ; cancer risk ; BINDING-PROTEINS ; DIET ; case-control studies ; DIABETES-MELLITUS ; EPIC ; nutrition ; FACTOR-I ; REGRESSION-MODELS ; physical activity ; BINDING PROTEIN ; insulin ; SERUM ; IGF-I ; ONCOLOGY ; BINDING-PROTEIN ; case-control study ; REGRESSION ; ASSOCIATIONS ; secretion ; BODY-SIZE ; PHYSICAL-ACTIVITY ; LEVEL ; biomarker ; case control studies ; pancreatic ; BLOOD-GLUCOSE ; INSULIN-RESISTANCE ; rectum ; USA ; prospective ; rectal cancer ; prospective study ; CANCERS ; CANCER-RISK ; C-PEPTIDE ; IGFBP-1 ; colorectal ; BINDING PROTEINS ; LOGISTIC-REGRESSION ; IGFBP-2 ; FACTOR BINDING PROTEIN-1 ; IGF ; insulin resistance ; GROWTH-FACTOR (IGF)-I
    Abstract: Western style diets and lifestyles are associated with increasing rates of obesity, diabetes and insulin resistance. Higher circulating insulin levels may modulate cell proliferation and apoptosis either directly or indirectly by increasing the bioactivity of IGF-I and decreasing the bioactivity of some of its binding proteins. The objective of this study was to determine the association of increasing levels of serum C-peptide, a biomarker of pancreatic insulin secretion, and IGF binding proteins (IGFBP) -1 and -2 with colorectal cancer risk in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC), a large cohort involving 10 Western European countries. A total of 1,078 colorectal cancer cases were matched (age, date of blood donation, fasting status, gender, study center) to an equal number of control subjects. Relative cancer risks were estimated using conditional logistic regression models. Serum C-peptide concentration was positively associated with an increased colorectal cancer risk for the highest versus the lowest quintile (OR = 1.56, 95% CI = 1.16-2.09, p(trend) 〈 0.01), which was slightly attenuated after adjustment for BMI and physical activity (OR = 1.37, 95% CI = 1.00-1.88, p(trend) = 0.10). When stratified by anatomical site, the cancer risk was stronger in the colon (OR 1.67, 95% CI = 1.14-2.46, p(trend) 〈 0.01) than in the rectum (OR 1.42, 95% CI = 0.90-2.25, p(trend) = 0.35). The cancer risk estimates were not heterogeneous by gender or fasting status. No clear colorectal cancer risk associations were observed for IGFBP-1 or -2. This large prospective study confirms that hyperinsulinemia, as determined by C-peptide levels, is associated with an increased colorectal cancer risk. (C) 2007 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17372899
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  • 7
    Keywords: CANCER ; COHORT ; RISK ; BREAST ; OVARIAN-CANCER ; WOMEN ; VALIDITY ; nutrition ; LIFE ; prospective ; ACTIVITY QUESTIONNAIRE
    Type of Publication: Journal article published
    PubMed ID: 19124520
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  • 8
    Keywords: CANCER ; BLOOD ; Germany ; MODEL ; MODELS ; FOLLOW-UP ; RISK ; RISKS ; METABOLISM ; TISSUE ; TIME ; RISK-FACTORS ; BINDING ; CYCLE ; ASSOCIATION ; BREAST-CANCER ; hormone ; resistance ; PLASMA ; AGE ; WOMEN ; OBESITY ; risk factors ; NECROSIS-FACTOR-ALPHA ; cancer risk ; case-control studies ; nutrition ; TYPE-2 ; ENDOMETRIAL CANCER ; RELATIVE RISK ; ADIPOSE-TISSUE ; POSTMENOPAUSAL WOMEN ; insulin ; case-control study ; REGRESSION ; ENDOMETRIAL ; MENSTRUAL-CYCLE ; fat distribution ; LEVEL ; case control studies ; INTERVAL ; methods ; PHASE ; INSULIN-RESISTANCE ; metabolic syndrome ; HORMONES ; PREMENOPAUSAL ; prospective ; RISK-FACTOR ; CANCER-RISK ; type 2 diabetes ; C-PEPTIDE ; SET ; SERUM ADIPONECTIN ; BINDING PROTEIN-1 ; CIRCULATING ADIPONECTIN
    Abstract: Background: Adiponectin, an adipocytokine secreted by adipose tissue, is decreased in obesity, insulin resistance, type 2 diabetes, and polycystic ovary syndrome, all of which are well-established risk factors for endometrial cancer. Methods: We conducted a case-control study nested within the European Prospective Investigation into Cancer and Nutrition to examine the relation between prediagnostic plasma adiponectin levels and endometrial cancer risk. Among pre- and postmenopausal women who were not currently using exogenous hormones, 284 women developed incident endometrial cancer during an average of 5.1 yr of follow-up. Using risk set sampling, 548 control subjects were selected, matched on center, age, menopausal status, phase of menstrual cycle, time of blood draw, and fasting status. Conditional logistic regression models were used to estimate relative risks and 95% confidence intervals. Results: Adiponectin levels were inversely associated with endometrial cancer risk [body mass index-adjusted relative risk for the top vs. bottom quartile = 0.56 (95% confidence interval 0.36-0.86), P-trend = 0.006]. There was evidence of a stronger inverse association among obese women than among nonobese women (P-heterogeneity = 0.03). The inverse association also appeared stronger for women who were postmenopausal or perimenopausal than premenopausal at baseline, but this was not statistically significantly heterogeneous (P-heterogeneity = 0.51). The association remained statistically significant after separate adjustment for other obesity-related physiological risk factors such as C-peptide, IGF binding protein-1, IGF binding protein-2, SHBG, estrone, or free testosterone but only marginally statistically significant after simultaneous adjustment for these factors. Conclusions: High circulating adiponectin levels are associated with reduced endometrial cancer risk, largely independent of other obesity-related risk factors
    Type of Publication: Journal article published
    PubMed ID: 17062769
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  • 9
    Keywords: CANCER ; GROWTH ; GROWTH-FACTOR ; MODEL ; MODELS ; FOLLOW-UP ; RISK ; RISKS ; PROTEIN ; SERA ; BINDING ; ASSOCIATION ; hormone ; WOMEN ; cancer risk ; case-control studies ; European Prospective Investigation into Cancer and Nutrition ; nutrition ; ENDOMETRIAL CANCER ; RELATIVE RISK ; POSTMENOPAUSAL WOMEN ; SERUM ; case-control study ; REGRESSION ; ENDOMETRIAL ; LEVEL ; case control studies ; INTERVAL ; SERUM-LEVELS ; HORMONES ; prospective ; RISK-FACTOR ; CANCER-RISK ; C-PEPTIDE ; IGFBP-1 ; SET ; IGFBP-2
    Abstract: We conducted a case-control study nested within the European Prospective Investigation into Cancer and Nutrition, to examine the associations between prediagnostic serum concentrations of C-peptide, insulin-like growth factor binding protein (IGFBP)-1 and IGFBP-2, and endometrial cancer risk. Among pre- and post-menopausal women, who were not currently using exogenous hormones, 286 women developed incident endometrial cancer during an average 5.1 years follow-up. Using risk set sampling, 555 matched control subjects were selected. In conditional logistic regression models adjusted for matching factors only, endometrial cancer risk increased with increasing serum levels of C-peptide (relative risks (RR) for the top vs. bottom quartile = 2.13 [95% confidence interval (CI) 1.33-3.41], p(trend) = 0.001, and decreasing serum levels of IGFBP-2 (RR for the top vs. bottom quartile = 0.56 [95% CI 0.35-0.90], p(trend) = 0.03, but was not significantly associated with IGFBP-1 levels (RR for the top vs. bottom quartile = 0.76 [95% CI 0.47-1.21], p(trend) = 0.25). In BMI-adjusted models, only the C-peptide association remained marginally statistically significant (RR for the top vs. bottom quartile = 1.56 [95% CI 0.94-2.57], p(trend) = 0.05 for C-peptide; 0.84 [95% CI 0.50-1.40], p(trend) = 0.74 for IGFBP-2; and 1.08 [95% CI 0.65-1.78], p(trend) = 0.86 for IGFBP-1 levels). These associations were stronger among nonfasting women (〈/=〈/=6 hr since last meal; 63% of subjects) but were not evident among fasting women, although the interactions were not statistically significant. The C-peptide-risk association was substantially attenuated after adjustment for free estradiol in postmenopausal women (RR for the top vs. bottom quartile = 1.28 [95% CI 0.67-2.45], p(trend) = 0.42. Our results provide modest support to the hypothesis that hyperinsulinaemia is a risk factor for endometrial cancer. (c) 2007 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17285578
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  • 10
    Keywords: CANCER ; THERAPY ; FOLLOW-UP ; RISK ; mechanisms ; ASSOCIATION ; hormone ; HEALTH ; AGE ; WOMEN ; etiology ; HORMONE REPLACEMENT THERAPY ; OBESITY ; risk factors ; cancer risk ; BODY ; nutrition ; ENDOMETRIAL CANCER ; LIFE-STYLE ; RELATIVE RISK ; OLDER WOMEN ; MASS INDEX ; ONCOLOGY ; ASSOCIATIONS ; ENDOMETRIAL ; WEIGHT ; PHYSICAL-ACTIVITY ; ADIPOSITY ; analysis ; methods ; anthropometry ; PREMENOPAUSAL WOMEN ; PREMENOPAUSAL ; prospective ; DIETARY ASSESSMENT METHODS ; INCREASED RISK ; CANCER-RISK ; BODY-FAT DISTRIBUTION ; ENDOGENOUS HORMONES ; BODY-MASS-INDEX ; IOWA WOMENS HEALTH ; SWEDISH TWIN REGISTRY ; WEIGHT CHANGE
    Abstract: Objective To examine the association between anthropometry and endometrial cancer, particularly by menopausal status and exogenous hormone use subgroups. Methods Among 223,008 women in the European Prospective Investigation into Cancer and Nutrition (EPIC) study, there were 567 incident endometrial cancer cases during 6.4 years of follow-up. The analysis was performed with Cox proportional hazards modeling. Results Weight, body mass index (BMI), waist and hip circumferences and waist-hip ratio (WHR) were strongly associated with increased risk of endometrial cancer. The relative risk (RR) for obese (BMI 30- 〈 40 kg/m(2)) compared to normal weight (BMI 〈 25) women was 1.78, 95% CI = 1.41-2.26, and for morbidly obese women (BMI 〉= 40) was 3.02, 95% CI = 1.66-5.52. The RR for women with a waist circumference of 〉= 88 cm vs. 〈 80 cm was 1.76, 95% CI = 1.42-2.19. Adult weight gain of 〉= 20 kg compared with stable weight (+/- 3 kg) increased risk independent of body weight at age 20 (RR = 1.75, 95% CI = 1.11-2.77). These associations were generally stronger for postmenopausal than premenopausal women, and oral contraceptives never-users than ever-users, and much stronger among never-users of hormone replacement therapy compared to ever-users. Conclusion Obesity, abdominal adiposity, and adult weight gain were strongly associated with endometrial cancer risk. These associations were particularly evident among never-users of hormone replacement therapy
    Type of Publication: Journal article published
    PubMed ID: 17297555
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