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  • POSTMENOPAUSAL WOMEN  (8)
  • 1
    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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  • 2
    Keywords: CANCER ; BLOOD ; Germany ; RISK ; METABOLISM ; ASSOCIATION ; BREAST-CANCER ; DESIGN ; NUMBER ; AGE ; WOMEN ; REPRODUCIBILITY ; etiology ; cancer risk ; EPIC ; nutrition ; ESTRADIOL ; POSTMENOPAUSAL WOMEN ; SERUM ; ONCOLOGY ; REGRESSION ; ESTROGEN ; LEVEL ; analysis ; PHASE ; PREMENOPAUSAL ; TESTOSTERONE ; prospective ; STEROID-HORMONES ; VARIABLES ; CANCER-RISK ; BINDING GLOBULIN ; ENGLAND ; steroids ; SEX-HORMONES ; postmenopausal ; androgens ; FREE TESTOSTERONE ; ESTROGENS
    Abstract: Epidemiological data show that reproductive and hormonal factors are involved in the etiology of endometrial cancer, but there is little data on the association with endogenous sex hormone levels. We analyzed the association between prediagnostic serum concentrations of sex steroids and endometrial cancer risk in the European Prospective Investigation into Cancer and Nutrition using a nested case-control design of 247 incident endometrial cancer cases and 481 controls, matched on center, menopausal status, age, variables relating to blood collection, and, for premenopausal women, phase of menstrual cycle. Using conditional regression analysis, endometrial cancer risk among postmenopausal women was positively associated with increasing levels of total testosterone, free testosterone, estrone, total estradiol, and free estradiol. The odds ratios (ORs) for the highest versus lowest tertile were 2.66 (95% confidence interval (CI) 1.50-4.72; P=0.002 for a continuous linear trend) for estrone, 2.07 (95% Cl 1.20-3.60; P=0.001) for estradiol, and 1.66 (95% Cl 0.98-2.82; P=0.001) for free estradiol. For total and free testosterone, ORs for the highest versus lowest tertile were 1.44 (95% Cl 0.88-2.36; P=0.05) and 2.05 (95% Cl 1.23-3.42; P=0.005) respectively. Androstenedione and dehydroepiandrosterone sulfate were not associated with risk. Sex hormone-binding globulin was significantly inversely associated with risk (OR for the highest versus lowest tertile was 0.57, 95% Cl 0.34-0.95; P=0.004). In premenopausal women, serum sex hormone concentrations were not clearly associated with endometrial cancer risk, but numbers were too small to draw firm conclusions. In conclusion, relatively high blood concentrations of estrogens and free testosterone are associated with an increased endometrial cancer risk in postmenopausal women
    Type of Publication: Journal article published
    PubMed ID: 18509001
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  • 3
    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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  • 4
    Keywords: OBESITY ; PATHOGENESIS ; nutrition ; ADIPOSE-TISSUE ; POSTMENOPAUSAL WOMEN ; GROWTH-FACTOR-I ; INSULIN-RESISTANCE ; PREMENOPAUSAL ; C-PEPTIDE ; Adiponectin
    Abstract: A "Western" lifestyle characterized by physical inactivity and excess weight is associated with a number of metabolic and hormonal dysregulations, including increased circulating estrogen levels, hyperinsulinemia, hyperglycemia, and chronic inflammation. The same hormonal and metabolic axes might mediate the association between this lifestyle and the development of endometrial cancer. Using data collected within the European Prospective Investigation into Cancer and Nutrition (EPIC), a prospective cohort study carried out in 10 European countries during 1992-2000, we conducted a factor analysis to delineate important components that summarize the variation explained by a set of biomarkers and to examine their association with endometrial cancer risk. Prediagnostic levels of testosterone, androstenedione, dehydroepiandrosterone sulfate, sex hormone-binding globulin, estrone, estradiol, C-peptide, insulin-like growth factor-binding proteins 1 and 2, adiponectin, high- and low-density lipoprotein cholesterol, glucose, triglycerides, tumor necrosis factor (TNF) alpha, soluble TNF receptors 1 and 2, C-reactive protein, interleukin-6, and interleukin-1 receptor antagonist were measured in 233 incident endometrial cancer cases and 446 matched controls. Factor analysis identified 3 components associated with postmenopausal endometrial cancer risk that could be labeled "insulin resistance/metabolic syndrome," "steroids," and "inflammation" factors. A fourth component, "lipids," was not significantly associated with endometrial cancer. In conclusion, besides the well-known associations of risk with sex hormones and insulin-regulated physiological axes, our data further support the hypothesis that inflammation factors play a role in endometrial carcinogenesis.
    Type of Publication: Journal article published
    PubMed ID: 23492765
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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: 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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  • 7
    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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  • 8
    Keywords: CANCER ; MODEL ; MODELS ; THERAPY ; FOLLOW-UP ; COHORT ; POPULATION ; RISK ; REDUCTION ; ASSOCIATION ; BREAST-CANCER ; NO ; hormone ; WOMEN ; etiology ; HORMONE REPLACEMENT THERAPY ; PROSPECTIVE COHORT ; cancer risk ; BODY ; EPIC ; nutrition ; ENDOMETRIAL CANCER ; LIFE-STYLE ; RELATIVE RISK ; POSTMENOPAUSAL WOMEN ; physical activity ; MASS INDEX ; ONCOLOGY ; ASSOCIATIONS ; ENDOMETRIAL ; PHYSICAL-ACTIVITY ; INTERVAL ; analysis ; ENERGY-BALANCE ; PREMENOPAUSAL WOMEN ; USA ; PREMENOPAUSAL ; prospective ; DIETARY ASSESSMENT METHODS ; CANCER-RISK ; ENDOGENOUS HORMONES ; ACTIVITY QUESTIONNAIRE ; BODY-MASS ; BODY-MASS-INDEX ; IOWA WOMENS HEALTH ; REPRODUCTIVE FUNCTION ; biologic mechanisms
    Abstract: The etiologic role of physical activity in endometrial cancer risk remains unclear given the few epidemiologic studies that have been conducted. To investigate this relation more fully, an analysis was,undertaken in the European prospective investigation into cancer and nutrition (EPIC). During an average 6.6 years of follow-up, 689 incident endometrial cancer cases were identified from an analytic cohort within EPIC of 253,023 women. Cox proportional hazards models were used to estimate the associations between type of activity (total, occupational, household, recreational) and endometrial cancer risk. For total activity, women in the highest compared with the lowest quartile of activity had a risk of 0.88 (95% confidence interval (95% CI = 0.61-1.27). No clear associations between each type of activity and endometrial cancer risk were found for the total study population combined. Associations were more evident in the stratified results, with premenopausal women who were active versus inactive experiencing a risk of 0.66 (95% CI = 0.38-1.14) overall. Among premenopausal women, for household and recreational activities the risk estimates in the highest as compared with the lowest quartiles were, respectively, 0.48 (95% CI = 0.23-0.99) and 0.78 (95% CI = 0.44-1.39). No effect modification by body mass index, hormone replacement therapy, oral contraceptive use or energy intake was found. This study provides no evidence of a protective effect of increased physical activity in endometrial cancer risk in all women but some support for a benefit among premenopausal women. The relative risk reductions are most apparent for household activities. (C) 2007 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17357139
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