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  • 1
    Keywords: EXPOSURE ; BIOMARKERS ; BREAST ; HUMANS ; smoking ; VALIDITY ; ENDOMETRIAL ; HEMOGLOBIN ADDUCTS ; glycidamide
    Abstract: Acrylamide, classified in 1994 by IARC as 'probably carcinogenic' to humans, was discovered in 2002 in some heat-treated, carbohydrate-rich foods. The association between dietary acrylamide intake and epithelial ovarian cancer risk (EOC) has been previously studied in one case-control and three prospective cohort studies which obtained inconsistent results, and could not further examine histological subtypes other than serous EOC. The present study was carried out in the European Prospective Investigation into Cancer and Nutrition (EPIC) sub-cohort of women (n=325,006). Multivariate Cox proportional hazards models were used to assess the association between questionnaire-based acrylamide intake and EOC risk. Acrylamide was energy-adjusted using the residual method, and was evaluated both as a continuous variable (per 10microg/day) and in quintiles; when subgroups by histological EOC subtypes were analyzed, acrylamide intake was evaluated in quartiles. During a mean follow-up of 11 years, 1,191 incident EOC cases were diagnosed. At baseline, the median acrylamide intake in EPIC was 21.3 mug/day. No associations, and no evidence for a dose-response were observed between energy-adjusted acrylamide intake and EOC risk (HR10microg/day:1.02, 95%CI:0.96-1.09; HRQ5vsQ1:0.97, 95%CI:0.76-1.23). No differences were seen when invasive EOC subtypes (582 serous, 118 endometrioid, and 79 mucinous tumors) were analyzed separately. This study did not provide evidence that acrylamide intake, based on food intake questionnaires, was associated with risk for EOC in EPIC. Additional studies with more reliable estimates of exposure based on biomarkers may be needed.
    Type of Publication: Journal article published
    PubMed ID: 25300475
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  • 2
    Keywords: CANCER ; BLOOD ; CELL-PROLIFERATION ; MODEL ; COHORT ; DISEASE ; RISK ; tumour ; ASSOCIATION ; PROGRESSION ; resistance ; PLASMA ; AGE ; MEN ; PROSPECTIVE COHORT ; prostate cancer ; PROSTATE-CANCER ; SWEDEN ; HIGH-LEVEL ; leptin ; insulin ; IGF-I ; ONCOLOGY ; REGRESSION ; RADICAL PROSTATECTOMY ; development ; GROWTH-FACTOR-I ; LEVEL ; case control studies ; INTERVAL ; INSULIN-RESISTANCE ; BODY-MASS INDEX ; USA ; prospective ; prospective study ; STEROID-HORMONES ; odds ratio ; C-PEPTIDE ; ANDROGEN ; prostatic neoplasms ; LOGISTIC-REGRESSION ; GENERAL-POPULATION ; insulin resistance ; FASTING GLUCOSE ; TYPE-2 DIABETES-MELLITUS ; blood glucose ; META-REGRESSION ANALYSIS ; SERUM LEPTIN LEVELS
    Abstract: Factors related to insulin resistance have been implicated in prostate cancer development, however, few analytical studies support such an association. We performed a case control study on 392 prostate cancer cases and 392 matched controls nested in a prospective cohort in Northern Sweden. Plasma concentrations of C-peptide, leptin, glycated haemoglobin (HbA1c) and fasting and post-load glucose were analysed and homeostatic model assessment of insulin resistance (HOMA-IR) was calculated. Conditional logistic regression analyses were used to calculate odds ratios (OR) of prostate cancer. High levels of C-peptide, HOMA-IR, leptin and HbA1c were associated with significant decreases in risk of prostate cancer, with ORs for top vs. bottom quartile for C-peptide of 0.59 (95% Confidence Interval [CI], 0.40-0.89; p(trend) = 0.008), HOMA-IR 0.60 (95% CI, 0.38-0.94; p(trend) = 0.03), leptin 0.55 (95% CI, 0.36-0.84; p(trend) = 0.006) and HbA1c 0.56 (95% CI, 0.35-0.91; p(trend) = 0.02). All studied factors were strongly inversely related to risk among men less than 59 years of age at blood sampling, but not among older men, with a significant heterogeneity between the groups for leptin (p(heterogeneity) = 0.006) and fasting glucose (p(heterogeneity) = 0.03). C-peptide and HOMA-IR were strongly inversely related to non-aggressive cancer but were non-significantly positively related to risk of aggressive disease (p(heterogeneity) = 0.007 and 0.01, respectively). Our data suggest that androgens, which are inversely associated with insulin resistance, are important in the early prostate cancer development, whereas insulin resistance related factors may be important for tumour progression. (c) 2007 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17278097
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  • 3
    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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  • 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
  • 6
    Keywords: CANCER ; BLOOD ; carcinoma ; COHORT ; cohort studies ; cohort study ; RISK ; ASSOCIATION ; HEALTH ; WOMEN ; OBESITY ; PROSPECTIVE COHORT ; COLORECTAL-CANCER ; SWEDEN ; CARCINOMAS ; body mass index ; REGRESSION ; ASSOCIATIONS ; WEIGHT ; BODY-SIZE ; GROWTH-FACTOR-I ; metabolic syndrome ; blood pressure ; SERUM-LEVELS ; prospective ; CORONARY HEART-DISEASE ; INCREASED RISK ; CANCERS ; CANCER-RISK ; CIRCULATING LEVELS ; C-PEPTIDE ; BODY-MASS ; endometrial neoplasms ; journals ; AGED NORWEGIAN MEN ; metabolic syndrome X
    Abstract: The authors examined the association between the metabolic syndrome and risk of incident endometnal and fatal uterine corpus cancer within a large prospective cohort study Approximately 290,000 women from Austria, Norway, and Sweden were enrolled during 1974-2005, with measurements of height, weight, systolic and diastolic blood pressure, and circulating levels of glucose, total cholesterol, and tnglycendes Relative risks were estimated using Cox proportional hazards regression. The metabolic syndrome was assessed as a composite z score, as the standardized sum of z scores for body mass index, blood pressure, glucose, cholesterol, and tnglycendes. A total of 917 endonnetnal carcinomas and 129 fatal cancers were identified Increased risks of incident endometnal carcinoma and fatal uterine corpus cancer were seen for the metabolic syndrome factors combined, as well as for individual factors (except for cholesterol) The relative risk of endometnal carcinoma for the metabolic syndrome was 1.37 (95% confidence interval 1 28, 1 46) per 1-unit increment of z score The positive associations between metabolic syndrome factors (both individually and combined) and endometrial carcinoma were confined to the heaviest women. The association between the metabolic syndrome and endometnal carcinoma risk seems to go beyond the risk conferred by obesity alone, particularly in women with a high body mass index
    Type of Publication: Journal article published
    PubMed ID: 20219764
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  • 7
    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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  • 8
    Keywords: FOLLOW-UP ; COHORT ; MORTALITY ; BLOOD-PRESSURE ; DIABETES-MELLITUS ; METAANALYSIS ; BODY-MASS INDEX ; CUTANEOUS MALIGNANT-MELANOMA ; BASAL-CELL CARCINOMA ; REGRESSION DILUTION
    Abstract: Background Little is known about the associations of metabolic aberrations with malignant melanoma (MM) and nonmelanoma skin cancer (NMSC). Objectives To assess the associations between metabolic factors (both individually and combined) and the risk of skin cancer in the large prospective Metabolic Syndrome and Cancer Project (Me-Can). Methods During a mean follow-up of 12 years of the Me-Can cohort, 1728 (41% women) incident MM, 230 (23% women) fatal MM and 1145 (33% women) NMSC were identified. Most NMSC cases (76%) were squamous cell carcinoma (SCC) (873, 33% women). Hazard ratios (HRs) were estimated by Cox proportional hazards regression for quintiles and standardized z-scores (with a mean of 0 and SD of 1) of body mass index (BMI), blood pressure, glucose, cholesterol, triglycerides and for a combined metabolic syndrome score. Risk estimates were corrected for random error in the measurements. Results Blood pressure per unit increase of z-score was associated with an increased risk of incident MM cases in men and women [HR 1.17, 95% confidence interval (CI) 1.04-1.31 and HR 1.18, 95% CI 1.03-1.36, respectively] and fatal MM cases among women (HR 2.39, 95% CI 1.58-3.64). In men, all quintiles for BMI above the reference were associated with a higher risk of incident MM. In women, SCC NMSC risk increased across quintiles for glucose levels (P-trend 0.02) and there was a trend with triglyceride concentration (P-trend 0.09). Conclusion These findings suggest that mechanisms linked to blood pressure may be involved in the pathogenesis of MM. SCC NMSC in women could be related to glucose and lipid metabolism.
    Type of Publication: Journal article published
    PubMed ID: 22530854
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  • 9
    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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  • 10
    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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