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  • COLON-CANCER  (4)
  • BODY-MASS INDEX  (2)
Keywords
  • 1
    Keywords: CELL LUNG-CANCER ; RISK ; PROSTATE-CANCER ; COLON-CANCER ; CALCIUM ; PHYSICAL-ACTIVITY ; VITAMIN-D-RECEPTOR ; SERUM 25-HYDROXYVITAMIN-D ; 1,25-DIHYDROXYVITAMIN D-3 ; SUPPLEMENT USE
    Abstract: BACKGROUND: Individuals with higher blood 25-hydroxyvitamin D [25(OH)D] levels have a lower risk of developing colorectal cancer (CRC), but the influence of 25(OH)D on mortality after CRC diagnosis is unknown. METHODS: The association between prediagnostic 25(OH)D levels and CRC-specific (N = 444) and overall mortality (N = 541) was prospectively examined among 1,202 participants diagnosed with CRC between 1992 and 2003 in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Multivariable Cox proportional hazards models were used to calculate HRs and corresponding 95% CIs according to 25(OH)D quintiles and genetic variation within the VDR and CASR genes. Potential dietary, lifestyle, and metabolic effect modifiers were also investigated. RESULTS: There were 541 deaths, 444 (82%) due to CRC. Mean follow-up was 73 months. In multivariable analysis, higher 25(OH)D levels were associated with a statistically significant reduction in CRC-specific (P(trend) = 0.04) and overall mortality (P(trend) = 0.01). Participants with 25(OH)D levels in the highest quintile had an adjusted HR of 0.69 (95% CI: 0.50-0.93) for CRC-specific mortality and 0.67 (95% CI: 0.50-0.88) for overall mortality, compared with the lowest quintile. Except for a possible interaction by prediagnostic dietary calcium intake (P(interaction) = 0.01), no other potential modifying factors related to CRC survival were noted. The VDR (FokI and BsmI) and CASR (rs1801725) genotypes were not associated with survival. CONCLUSIONS: High prediagnostic 25(OH)D levels are associated with improved survival of patients with CRC. Impact: Our findings may stimulate further research directed at investigating the effects of blood vitamin D levels before, at, and after CRC diagnosis on outcomes in CRC patients. Cancer Epidemiol Biomarkers Prev; 21(4); 582-93. (c)2012 AACR.
    Type of Publication: Journal article published
    PubMed ID: 22278364
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  • 2
    Keywords: GENES ; PLASMA ; WOMEN ; OBESITY ; COLON-CANCER ; ADIPOSE-TISSUE ; RECTAL-CANCER ; CORONARY-HEART-DISEASE ; METAANALYSIS ; metabolic syndrome
    Abstract: Adiponectin-an adipose tissue-derived protein-may provide a molecular link between obesity and colorectal cancer (CRC), but evidence from large prospective studies is limited. In particular, no epidemiological study explored high-molecular weight (HMW) and non-HMW adiponectin fractions in relation to CRC risk, despite them being hypothesized to have differential biological activities, i.e. regulating insulin sensitivity (HMW adiponectin) versus inflammatory response (non-HMW adiponectin). In a prospective, nested case-control study, we investigated whether prediagnostic serum concentrations of total, HMW and non-HMW adiponectin are associated with risk of CRC, independent of obesity and other known CRC risk factors. A total of 1206 incident cases (755 colon and 451 rectal) were matched to 1206 controls using incidence-density sampling. In conditional logistic regression, adjusted for dietary and lifestyle factors, total adiponectin and non-HMW adiponectin concentrations were inversely associated with risk of CRC [relative risk (RR) comparing highest versus lowest quintile = 0.71, 95% confidence interval (CI) = 0.53-0.95, P(trend) = 0.03 for total adiponectin and RR = 0.45, 95% CI = 0.34-0.61, P(trend) 〈 0.0001 for non-HMW adiponectin]. HMW adiponectin concentrations were not associated with CRC risk (RR = 0.91, 95% CI = 0.68-1.22, P(trend) = 0.55). Non-HMW adiponectin was associated with CRC risk even after adjustment for body mass index and waist circumference (RR = 0.39, 95% CI = 0.26-0.60, P(trend) 〈 0.0001), whereas the association with total adiponectin was no longer significant (RR = 0.81, 95% CI = 0.60-1.09, P(trend) = 0.23). When stratified by cancer site, non-HMW adiponectin was inversely associated with both colon and rectal cancer. These findings suggest an important role of the relative proportion of non-HMW adiponectin in CRC pathogenesis. Future studies are warranted to confirm these results and to elucidate the underlying mechanisms.
    Type of Publication: Journal article published
    PubMed ID: 22431719
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  • 3
    Keywords: CANCER ; BLOOD ; Germany ; THERAPY ; RISK ; RISKS ; PROTEIN ; colon ; CYCLE ; ASSOCIATION ; hormone ; HEALTH ; resistance ; AGE ; WOMEN ; MEN ; OBESITY ; smoking ; COLORECTAL-CANCER ; cancer risk ; COLON-CANCER ; cholesterol ; C-REACTIVE PROTEIN ; body mass index ; nutrition ; education ; NESTED CASE-CONTROL ; CROHNS-DISEASE ; inflammation ; insulin ; SERUM ; case-control study ; REGRESSION ; ASSOCIATIONS ; colon cancer ; METAANALYSIS ; PHASE ; INSULIN-RESISTANCE ; metabolic syndrome ; REPLACEMENT THERAPY ; prospective ; CANCER-RISK ; colorectal neoplasms ; C-PEPTIDE ; REPLACEMENT ; WAIST CIRCUMFERENCE ; INFLAMMATORY MARKERS ; nested case-control study ; BODY-MASS ; COLLECTION ; HORMONE-THERAPY ; Abdominal ; Hyperinsulinism ; journals ; nested case control study ; hyperglycemia ; hyperlipidemias
    Abstract: The authors investigated associations between serum C-reactive protein (CRP) concentrations and colon and rectal cancer risk in a nested case-control study within the European Prospective Investigation into Cancer and Nutrition (1992-2003) among 1,096 incident cases and 1,096 controls selected using risk-set sampling and matched on study center, age, sex, time of blood collection, fasting status, menopausal status, menstrual cycle phase, and hormone replacement therapy. In conditional logistic regression with adjustment for education, smoking, nutritional factors, body mass index, and waist circumference, CRP showed a significant nonlinear association with colon cancer risk but not rectal cancer risk. Multivariable-adjusted relative risks for CRP concentrations of 〉= 3.0 mg/L versus 〈 1.0 mg/L were 1.36 (95% confidence interval (CI): 1.00, 1.85; P-trend = 0.01) for colon cancer and 1.02 (95% CI: 0.67, 1.57; P-trend = 0.65) for rectal cancer. Colon cancer risk was significantly increased in men (relative risk = 1.74, 95% CI: 1.11, 2.73; P-trend = 0.01) but not in women (relative risk = 1.06, 95% CI: 0.67, 1.68; P-trend = 0.13). Additional adjustment for C-peptide, glycated hemoglobin, and high density lipoprotein cholesterol did not attenuate these results. These data provide evidence that elevated CRP concentrations are related to a higher risk of colon cancer but not rectal cancer, predominantly among men and independently of obesity, insulin resistance, and dyslipidemia
    Type of Publication: Journal article published
    PubMed ID: 20634278
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  • 4
    Keywords: CANCER ; COHORT ; POPULATION ; RISK ; RISK-FACTORS ; ASSOCIATION ; OBESITY ; COLON-CANCER ; nutrition ; IGF-I ; SERUM-LEVELS ; VITAMIN-D STATUS ; CALCIUM-SENSING RECEPTOR ; PRIMARY HYPERPARATHYROIDISM ; PTH/PTHRP RECEPTOR
    Abstract: Background: Parathyroid hormone (PTH) has been proposed to play a promoting role in carcinogenesis. However, no epidemiologic studies have yet directly investigated its role in colorectal cancer (CRC). Methods: A case-control study nested within the European Prospective Investigation into Cancer and Nutrition cohort was conducted with 1,214 incident, sporadic CRC cases matched to 1,214 controls. Circulating prediagnostic PTH and 25-hydroxy vitamin D [25(OH) D] concentrations were measured by enzyme-linked immunosorbent assays. Detailed dietary and lifestyle questionnaire data were collected at baseline. Multivariable conditional logistic regression was used to estimate the incidence rate ratio (RR) with 95% confidence intervals (95% CI) for the association between circulating PTH and CRC risk. Results: In multivariate analyses [including adjustment for 25(OH) D concentration] with a priori defined cutoff points, high levels of serum PTH (〉= 65 ng/L) compared with medium PTH levels of 30-65 ng/L were associated with increased CRC risk (RR = 1.41,95% CI: 1.03-1.93). In analyses by sex, the CRC risk was 1.77 (95% CI: 1.14-2.75) and 1.15 (95% CI: 0.73-1.84) in men and women, respectively (P-heterogeneity = 0.01). In subgroup analyses by anatomical subsite, the risk for colon cancer was RR = 1.56, 95% CI: 1.03-2.34, and for rectal cancer RR = 1.20, 95% CI: 0.72-2.01 (P-heterogeneity = 0.21). Effect modification by various risk factors was examined. Conclusions: The results of this study suggest that high serum PTH levels may be associated with incident, sporadic CRC in Western European populations, and in particular among men. Impact: To our knowledge, this is the first study on PTH and CRC. The role of PTH in carcinogenesis needs to be further investigated.
    Type of Publication: Journal article published
    PubMed ID: 21378267
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  • 5
    Keywords: COHORT ; WOMEN ; OBESITY ; NON-HODGKINS-LYMPHOMA ; PHYSICAL-ACTIVITY ; BODY-MASS INDEX ; ALL-CAUSE MORTALITY ; OVERWEIGHT ; LYMPHOHEMATOPOIETIC MALIGNANCIES ; ADULT LEUKEMIA
    Abstract: PURPOSE: Overweight and obesity have been suggested as a risk factor for leukemia. Impaired immune function associated with obesity, increased insulin-like growth factor-I activity and stimulating effects of leptin suggest a possible biological link between anthropometric measures and leukemia. However, evidence from epidemiological studies has been inconsistent. We examined the potential association between prospective measurements of body size and risk of leukemia among participants of the European Prospective Investigation into Cancer and Nutrition (EPIC). METHODS: During follow-up (mean = 11.52 years, standard deviation = 2.63), 671 leukemia (lymphoid leukemia = 50.1 %, myeloid leukemia = 43.2 %) cases were identified. Anthropometric measures including weight, height, body mass index (BMI), waist circumference (WC), hip circumference, and waist-to-hip ratio (WHR) were measured. Cox proportional hazard models were used to explore the association between anthropometric measures and risk of leukemia. RESULTS: No associations were observed between anthropometric measures and total leukemia, and lymphoid leukemia. Risk of myeloid leukemia significantly increased for higher categories of BMI and WC among women. Analyses by subtype of myeloid leukemia showed an increased risk of acute myeloid leukemia (AML) for higher categories of WHR among women. This association seemed to be reversed for chronic myeloid leukemia. No association between anthropometric measures and myeloid leukemia were observed among men except an increased risk of AML with height. CONCLUSION: The study showed no associations between anthropometric measures and total leukemia, and lymphoid leukemia among men and women. A possible association between BMI as general obesity and WC as abdominal obesity and increased risk of myeloid leukemia among women were observed.
    Type of Publication: Journal article published
    PubMed ID: 23288400
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  • 6
    Keywords: COHORT ; HEALTH ; OBESITY ; COLORECTAL-CANCER ; nutrition ; REGRESSION ; PHYSICAL-ACTIVITY ; SIZE ; BODY-MASS INDEX ; COMPETING RISKS
    Abstract: BACKGROUND: A moderate association exists between body mass index (BMI) and colorectal cancer. Less is known about the effect of weight change. OBJECTIVE: We investigated the relation between BMI and weight change and subsequent colon and rectal cancer risk. DESIGN: This was studied among 328,781 participants in the prospective European Prospective Investigation into Cancer-Physical Activity, Nutrition, Alcohol, Cessation of Smoking, Eating study (mean age: 50 y). Body weight was assessed at recruitment and on average 5 y later. Self-reported weight change (kg/y) was categorized in sex-specific quintiles, with quintiles 2 and 3 combined as the reference category (men: -0.6 to 0.3 kg/y; women: -0.4 to 0.4 kg/y). In the subsequent years, participants were followed for the occurrence of colon and rectal cancer (median period: 6.8 y). Multivariable Cox proportional hazards regression analyses were used to study the association. RESULTS: A total of 1261 incident colon cancer and 747 rectal cancer cases were identified. BMI at recruitment was statistically significantly associated with colon cancer risk in men (HR: 1.04; 95% CI: 1.02, 1.07). Moderate weight gain (quintile 4) in men increased risk further (HR: 1.32; 95% CI: 1.04, 1.68), but this relation did not show a clear trend. In women, BMI or weight gain was not related to subsequent risk of colon cancer. No statistically significant associations for weight loss and colon cancer or for BMI and weight changes and rectal cancer were found. CONCLUSIONS: BMI attained at adulthood was associated with colon cancer risk. Subsequent weight gain or loss was not related to colon or rectal cancer risk in men or women.
    Type of Publication: Journal article published
    PubMed ID: 24225355
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