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  • EPIDEMIOLOGY  (7)
  • 1
    Keywords: CANCER ; tumor ; PROSTATE ; COHORT ; EPIDEMIOLOGY ; RISK ; METABOLISM ; TUMORS ; BINDING ; ASSOCIATION ; NO ; hormone ; PLASMA ; prostate cancer ; PROSTATE-CANCER ; SWEDEN ; cancer risk ; case-control studies ; HIGH-LEVEL ; SERUM ; case control study ; case-control study ; ASSOCIATIONS ; INCREASE ; TUMORIGENESIS ; RADICAL PROSTATECTOMY ; prospective studies ; LEVEL ; case control studies ; methods ; PLASMA-LEVELS ; USA ; HORMONES ; TESTOSTERONE ; prospective ; prospective study ; STEROID-HORMONES ; odds ratio ; CANCER-RISK ; CIRCULATING LEVELS ; ANDROGEN ; prostatic neoplasms ; androgens ; ENDOGENOUS SEX-HORMONES ; ANDROSTANEDIOL GLUCURONIDE ; FREE TESTOSTERONE ; PLASMA TESTOSTERONE
    Abstract: BACKGROUND. Androgens have been implicated in prostate tumorigenesis, but prospective studies have overall reported no association between circulating levels of androgens and risk of prostate cancer. However, some recent studies have shown that a high level of testosterone increase the risk of non-aggressive tumors but is associated with a decreased risk of aggressive tumors. METHODS. We prospectively measured plasma levels of total testosterone, androstanediol glucuronide (A-diol-g) and sex hormone binding globuline (SHBG) and calculated estimated levels of free testosterone, in a nested case-control study of 392 cases and 392 matched controls. RESULTS. None of the studied hormones were significantly associated with prostate cancer risk in the full study group or in subgroups according to tumor aggressiveness. Odds ratios in the full study group, for top versus bottom quartile, was for total testosterone 1.25 (95% Cl = 0.79-2.00; P-trend = 0.51); free testosterone, 1.31 (95% Cl = 0.82-2.07; P-trend = 0.35); A-diol-g, 0.88 (95% Cl = 0.59-1.33; P-trend = 0.77); and for SHBG, 1.01 (95% Cl = 0.64-1.58; P-trend = 0.94). CONCLUSIONS. We found no significant associations between androgen levels and risk of prostate cancer in this population-based, non-screened cohort. Prostate 67: 1230-1237, 2007. (c) 2007 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17562541
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  • 2
    Keywords: cohort study ; EPIDEMIOLOGY ; HEPATOCELLULAR-CARCINOMA ; hepatocellular carcinoma ; UNITED-STATES ; DIABETES-MELLITUS ; ALCOHOL-CONSUMPTION ; INCIDENCE RATES ; VIRUS-INFECTION ; metabolic syndrome ; US ADULTS ; REGRESSION DILUTION ; INTERNATIONAL TRENDS ; intrahepatic cholangiocarcinoma ; TOTAL SERUM-CHOLESTEROL
    Abstract: Initial studies have indicated diabetes and obesity to be risk factors for hepatocellular carcinoma; but the association between other metabolic risk factors and primary liver cancer (PLC) has not been investigated. The metabolic syndrome and cancer project (Me-Can) includes cohorts from Norway, Austria and Sweden with data on 578,700 subjects. We used Cox proportional hazard models to calculate relative risks (RRs) of PLC by body mass index (BMI), blood pressure and plasma levels of glucose, cholesterol and triglycerides as continuous standardized variables (z-score with mean = 0 and standard deviation (SD) = 1) and their standardized sum of metabolic syndrome (MetS) z-score. RRs were corrected for random error in measurements. During an average follow-up of 12.0 years (SD = 7.8), 266 PLCs were diagnosed among cohort members. RR of liver cancer per unit increment of z-score adjusted for age, smoking status and BMI and stratified by birth year, sex and sub-cohorts, was for BMI 1.39 (95% confidence interval (CI) 1.24-1.58), mid blood pressure 2.08 (0.95-4.73), blood glucose 2.13 (1.55-2.94) cholesterol 0.62 (0.51-0.76) and serum triglycerides 0.85 (0.65-1.10). The RR per one unit increment of the MetS z-score was 1.35 (1.12-1.61). BMI, glucose and a composite MetS score were positively and cholesterol negatively associated with risk of liver cancer.
    Type of Publication: Journal article published
    PubMed ID: 21805476
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  • 3
    Keywords: COHORT ; EPIDEMIOLOGY ; WOMEN ; COUNTRIES ; DIET ; DRINKING ; CELL CARCINOMA ; METAANALYSIS ; KIDNEY CANCER ; FLUID INTAKE
    Abstract: Epidemiologic studies have reported that moderate alcohol consumption is inversely associated with the risk of renal cancer. However, there is no information available on the associations in renal cancer subsites. From 1992 through to 2010, 477,325 men and women in the European Prospective Investigation into Cancer and Nutrition cohort were followed for incident renal cancers (n = 931). Baseline and lifetime alcohol consumption was assessed by country-specific, validated dietary questionnaires. Information on past alcohol consumption was collected by lifestyle questionnaires. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated from Cox proportional hazard models. In multivariate analysis, total alcohol consumption at baseline was inversely associated with renal cancer; the HR and 95% CI for the increasing categories of total alcohol consumption at recruitment versus the light drinkers category were 0.78 (0.62-0.99), 0.82 (0.64-1.04), 0.70 (0.55-0.90), 0.91 (0.63-1.30), respectively, (ptrend = 0.001). A similar relationship was observed for average lifetime alcohol consumption and for all renal cancer subsites combined or for renal parenchyma subsite. The trend was not observed in hypertensive individuals and not significant in smokers. In conclusion, moderate alcohol consumption was associated with a decreased risk of renal cancer.
    Type of Publication: Journal article published
    PubMed ID: 25866035
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  • 4
    Keywords: CANCER ; BLOOD ; EPIDEMIOLOGY ; RISK-FACTORS ; FREQUENCY ; LYMPHOCYTES ; B-CELL LYMPHOMA ; NON-HODGKINS-LYMPHOMA ; SUBTYPES ; HEALTHY-INDIVIDUALS
    Abstract: PURPOSE: The strong association between t(14;18) translocation and follicular lymphoma (FL) is well known. However, the determinants of this chromosomal aberration and their role in t(14;18) associated FL remain to be established. METHODS: t(14;18) frequency within the B cell lymphoma 2 major breakpoint region was determined for 135 incident FL cases and 251 healthy controls as part of a nested case-control study within the European Prospective Investigation into Cancer cohort. Quantitative real-time PCR was performed in DNA extracted from blood samples taken at recruitment. The relationship between prevalence and frequency of the translocation with baseline anthropometric, lifestyle, and dietary factors in cases and controls was determined. Unconditional logistic regression was used to explore whether the risk of FL associated with these factors differed in t(14;18)(+) as compared to t(14;18)(-) cases. RESULTS: Among incident FL cases, educational level (chi (2) p = 0.021) and height (chi (2) p = 0.025) were positively associated with t(14;18) prevalence, and cases with high frequencies [t(14;18)(HF)] were significantly taller (t test p value = 0.006). These findings were not replicated in the control population, although there were a number of significant associations with dietary variables. Further analyses revealed that height was a significant risk factor for t(14;18)(+) FL [OR 6.31 (95 % CI 2.11, 18.9) in the tallest versus the shortest quartile], but not t(14;18)(-) cases. CONCLUSIONS: These findings suggest a potential role for lifestyle factors in the prevalence and frequency of the t(14;18) translocation. The observation that the etiology of FL may differ by t(14;18) status, particularly with regard to height, supports the subdivision of FL by translocation status.
    Type of Publication: Journal article published
    PubMed ID: 26424368
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  • 5
    Keywords: CANCER ; carcinoma ; COHORT ; EPIDEMIOLOGY ; RISK ; OBESITY ; HUMAN-PAPILLOMAVIRUS ; cholesterol ; METAANALYSIS ; VULVAR CANCER ; COMPLETENESS ; REGRESSION DILUTION ; COFACTORS ; MetS ; rare gynecological cancers
    Abstract: Background: Risk factors for rare gynecological cancers are largely unknown. Initial research has indicated that the metabolic syndrome (MetS) or individual components could play a role. Materials and methods: The Metabolic syndrome and Cancer project cohort includes 288 834 women. During an average follow-up of 11 years, 82 vulvar, 26 vaginal and 43 other rare gynecological cancers were identified. Hazard ratios (HRs) were estimated fitting Cox proportional hazards regression models for tertiles and standardized z-scores [with a mean of 0 and a standard deviation (SD) of 1] of body mass index (BMI), blood pressure, glucose, cholesterol, triglycerides and MetS. Risk estimates were corrected for random error in the measurement of metabolic factors. Results: The MetS was associated with increased risk of vulvar [HR 1.78, 95% confidence interval (CI) 1.30-2.41) and vaginal cancer (HR 1.87, 95% CI 1.07-3.25). Among separate MetS components, 1 SD increase in BMI was associated with overall risk (HR 1.43, 95% CI 1.23-1.66), vulvar (HR 1.36, 95% CI 1.11-1.69) and vaginal cancer (HR 1.79, 95% CI 1.30-2.46). Blood glucose and triglyceride concentrations were associated with increased risk of vulvar cancer (HR 1.98, 95% CI 1.10-3.58 and HR 2.09, 95% CI 1.39-3.15, respectively). Conclusion: The results from this first prospective study on rare gynecological cancers suggest that the MetS and its individual components may play a role in the development of these tumors
    Type of Publication: Journal article published
    PubMed ID: 20966183
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  • 6
    Keywords: CANCER ; GROWTH-FACTOR ; carcinoma ; COHORT ; EPIDEMIOLOGY ; RISK ; RISK-FACTORS ; score ; WOMEN ; OBESITY ; cervical cancer ; HUMAN-PAPILLOMAVIRUS ; SQUAMOUS-CELL CARCINOMA ; adenocarcinoma ; UTERINE CERVIX ; PROJECT ; metabolic syndrome ; COMPLETENESS ; REGRESSION DILUTION ; CONOR ; Squamous cell ; Metabolic factors
    Abstract: Background. Little is known about the association between metabolic risk factors and cervical cancer carcinogenesis. Material and methods. During mean follow-up of 11 years of the Me-Can cohort (N = 288,834) 425 invasive cervical cancer cases were diagnosed. Hazard ratios (HRs) were estimated by the use of Cox proportional hazards regression models for quintiles and standardized z-scores (with a mean of 0 and a SD of 1) of BMI, blood pressure, glucose, cholesterol, triglycerides and MetS score. Risk estimates were corrected for random error in the measurements. Results. BMI (per 1SD increment) was associated with 12%, increase of cervical cancer risk, blood pressure with 25% and triglycerides with 39%, respectively. In models including all metabolic factors, the associations for blood pressure and triglycerides persisted. The metabolic syndrome (MetS) score was associated with 26% increased corrected risk of cervical cancer. Triglycerides were stronger associated with squamous cell carcinoma (HR 1.48; 95% CI, 1.20-1.83) than with adenocarcinoma (0.92, 0.54-1.56). Among older women cholesterol (50-70 years 1.34; 1.00-1.81), triglycerides (50-70 years 1.49, 1.03-2.16 and 〉= 70 years 1.54, 1.09-2.19) and glucose (〉= 70 years 1.87, 1.13-3.11) were associated with increased cervical cancer risk. Conclusion. The presence of obesity, elevated blood pressure and triglycerides were associated with increased risk of cervical cancer.
    Type of Publication: Journal article published
    PubMed ID: 22330614
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  • 7
    Keywords: CANCER ; COHORT ; cohort studies ; EPIDEMIOLOGY ; RISK ; ASSOCIATION ; WOMEN ; OBESITY ; cholesterol ; BLOOD-PRESSURE ; ADULTS ; METAANALYSIS ; blood pressure ; BODY-MASS INDEX ; OVERWEIGHT ; colorectal neoplasms ; INDIVIDUAL DATA ; blood glucose ; INSULIN-RESISTANCE SYNDROME ; metabolic syndrome X ; REGRESSION DILUTION ; triglycerides ; VASCULAR MORTALITY
    Abstract: BACKGROUND: The metabolic syndrome (MetS) has been related to an increased risk of colorectal cancer, but the modest size of previous studies precluded detailed characterization of the role of individual MetS factors and their interaction on risk. METHODS: In the Metabolic Syndrome and Cancer Project (Me-Can), data on body mass index (BMI), blood pressure, and blood levels of glucose, cholesterol, and triglycerides were available for 578,700 men and women. The mean age of participants at baseline was 44 years, and the mean follow-up was 12 years. Relative risks (RR) of colorectal cancer per 1 standard deviation increment in Z score of factors and for a combined MetS score, were calculated from Cox regression models, including adjustment for potential confounders. RESULTS: During follow-up, 2834 men and 1861 women were diagnosed with colorectal cancer. The RR of colorectal cancer for the MetS score was 1.25 (95% confidence interval [CI], 1.18-1.32) in men, and 1.14 (95% CI, 1.06-1.22) in women. Significant associations also were observed in men for BMI (RR, 1.07; 95% CI, 1.02-1.13), blood pressure (RR, 1.10; 95% CI, 1.02-1.18), and triglycerides (RR, 1.17; 95% CI, 1.06-1.28) and, in women, for BMI (RR, 1.08; 95% CI, 1.01-1.15). There was no significant positive interaction between the metabolic factors on risk. CONCLUSIONS: The combination of metabolic factors and some separate factors was related to an increased risk of colorectal cancer, but there was no interaction between metabolic factors.
    Type of Publication: Journal article published
    PubMed ID: 21171019
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