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  • 1
    Keywords: CANCER ; MODEL ; MODELS ; SUPPORT ; COHORT ; DEATH ; DISEASE ; EXPOSURE ; MORTALITY ; RISK ; TIME ; POLYMORPHISMS ; hippocampus ; CARE ; CIGARETTE-SMOKING ; smoking ; RATES ; DAMAGE ; RISK FACTOR ; PREVALENCE ; LIPID-PEROXIDATION ; CONSUMPTION ; EPIC ; nutrition ; CORTEX ; USA ; prospective ; INCREASED RISK ; RISK-FACTOR ; lipid ; amyotrophic lateral sclerosis ; INVESTIGATE ; 33 ; FORMALDEHYDE ; SPORADIC ALS
    Abstract: Objective: Cigarette smoking has been reported as "probable" risk factor for Amyotrophic Lateral Sclerosis (ALS), a poorly understood disease in terms of aetiology. The extensive longitudinal data of the European Prospective Investigation into Cancer and Nutrition (EPIC) were used to evaluate age-specific mortality rates from ALS and the role of cigarette smoking on the risk of dying from ALS. Methods: A total of 517,890 healthy subjects were included, resulting in 4,591,325 person-years. ALS cases were ascertained through death certificates. Cox hazard models were built to investigate the role of smoking on the risk of ALS, using packs/years and smoking duration to study dose-response. Results: A total of 118 subjects died from ALS, resulting in a crude mortality rate of 2.69 per 100,000/year. Current smokers at recruitment had an almost two-fold increased risk of dying from ALS compared to never smokers (HR = 1.89, 95% C.I. 1.14-3.14), while former smokers at the time of enrolment had a 50% increased risk (HR = 1.48, 95% C.I. 0.94-2-32). The number of years spent smoking increased the risk of ALS (p for trend = 0.002). Those who smoked more than 33 years had more than a two-fold increased risk of ALS compared with never smokers (HR = 2.16, 95% C.I. 1.33-3.53). Conversely, the number of years since quitting smoking was associated with a decreased risk of ALS compared with continuing smoking. Interpretation: These results strongly support the hypothesis of a role of cigarette smoking in aetiology of ALS. We hypothesize that this could occur through lipid peroxidation via formaldehyde exposure. Ann Neurol 2009;65:378-385
    Type of Publication: Journal article published
    PubMed ID: 19399866
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  • 2
    Keywords: SURVIVAL ; MORTALITY ; OBESITY ; smoking ; REGRESSION-MODELS ; MASS INDEX ; OVERWEIGHT ; ALS PATIENTS ; NUTRITIONAL-STATUS ; HYPERMETABOLISM
    Abstract: OBJECTIVES: The aim of this study was to investigate for the first time the association between body fat and risk of amyotrophic lateral sclerosis (ALS) with an appropriate prospective study design. METHODS: The EPIC (European Prospective Investigation into Cancer and Nutrition) study included 518,108 individuals recruited from the general population across 10 Western European countries. At recruitment, information on lifestyle was collected and anthropometric characteristics were measured. Cox hazard models were fitted to investigate the associations between anthropometric measures and ALS mortality. RESULTS: Two hundred twenty-two ALS deaths (79 men and 143 women) occurred during the follow-up period (mean follow-up = 13 years). There was a statistically significant interaction between categories of body mass index and sex regarding ALS risk (p = 0.009): in men, a significant linear decrease of risk per unit of body mass index was observed (hazard ratio = 0.93, 95% confidence interval 0.86-0.99 per kg/m(2)); among women, the risk was more than 3-fold increased for underweight compared with normal-weight women. Among women, a significant risk reduction increasing the waist/hip ratio was also evident: women in the top quartile had less than half the risk of ALS compared with those in the bottom quartile (hazard ratio = 0.48, 95% confidence interval 0.25-0.93) with a borderline significant p value for trend across quartiles (p = 0.056). CONCLUSION: Increased prediagnostic body fat is associated with a decreased risk of ALS mortality.
    Type of Publication: Journal article published
    PubMed ID: 23390184
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  • 3
    Keywords: MORTALITY ; COUNTRIES ; SWEDEN ; METAANALYSIS ; SUBTYPES ; LYMPHOHEMATOPOIETIC MALIGNANCIES ; BENZENE EXPOSURE ; MYELOGENOUS LEUKEMIA ; INDUSTRY WORKERS ; CHEMISTS
    Abstract: OBJECTIVES: Established risk factors for leukaemia do not explain the majority of leukaemia cases. Previous studies have suggested the importance of occupation and related exposures in leukaemogenesis. We evaluated possible associations between job title and selected hazardous agents and leukaemia in the European Prospective Investigation into Cancer and Nutrition. METHODS: The mean follow-up time for 241 465 subjects was 11.20 years (SD 2.42 years). During the follow-up period, 477 incident cases of myeloid and lymphoid leukaemia occurred. Data on 52 occupations considered a priori to be at high risk of developing cancer were collected through standardised questionnaires. Occupational exposures were estimated by linking the reported occupations to a job exposure matrix. Cox proportional hazard models were used to explore the association between occupation and related exposures and risk of leukaemia. RESULTS: The risk of lymphoid leukaemia significantly increased for working in chemical laboratories (HR 8.35, 95% CI 1.58 to 44.24), while the risk of myeloid leukaemia increased for working in the shoe or other leather goods industry (HR 2.54, 95% CI 1.28 to 5.06). Exposure-specific analyses showed a non-significant increased risk of myeloid leukaemias for exposure to benzene (HR 1.15, 95% CI 0.75 to 1.40; HR=1.60, 95% CI 0.95 to 2.69 for the low and high exposure categories, respectively). This association was present both for acute and chronic myeloid leukaemia at high exposure levels. However, numbers were too small to reach statistical significance. CONCLUSIONS: Our findings suggest a possible role of occupational exposures in the development of both lymphoid and myeloid leukaemia. Exposure to benzene seemed to be associated with both acute and chronic myeloid leukaemia.
    Type of Publication: Journal article published
    PubMed ID: 23576671
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  • 4
    Keywords: neoplasms ; COHORT ; MORTALITY ; WORKERS ; METAANALYSIS ; CANCER INCIDENCE ; ORGANIC-SOLVENTS ; EPILYMPH ; EPIDEMIOLOGY CONSORTIUM INTERLYMPH
    Abstract: OBJECTIVES: We evaluated the association between occupational exposure to trichloroethylene (TCE) and risk of non-Hodgkin lymphoma (NHL) in a pooled analysis of four international case-control studies. METHODS: Overall, the pooled study population included 3788 NHL cases and 4279 controls. Risk of NHL and its major subtypes associated with TCE exposure was calculated with unconditional logistic regression and polytomous regression analysis, adjusting by age, gender and study. RESULTS: Risk of follicular lymphoma (FL), but not NHL overall or other subtypes, increased by probability (p=0.02) and intensity level (p=0.04), and with the combined analysis of four exposure metrics assumed as independent (p=0.004). After restricting the analysis to the most likely exposed study subjects, risk of NHL overall, FL and chronic lymphocytic leukaemia (CLL) were elevated and increased by duration of exposure (p=0.009, p=0.04 and p=0.01, respectively) and with the combined analysis of duration, frequency and intensity of exposure (p=0.004, p=0.015 and p=0.005, respectively). Although based on small numbers of exposed, risk of all the major NHL subtypes, namely diffuse large B-cell lymphoma, FL and CLL, showed increases in risk ranging 2-3.2-fold in the highest category of exposure intensity. No significant heterogeneity in risk was detected by major NHL subtypes or by study. CONCLUSIONS: Our pooled analysis apparently supports the hypothesis of an increase in risk of specific NHL subtypes associated with occupational exposure to TCE.
    Type of Publication: Journal article published
    PubMed ID: 23881218
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  • 5
    Keywords: CANCER ; EPIDEMIOLOGY ; MORTALITY ; RISK ; INFECTION ; IMPACT ; BIOMARKERS ; ASSOCIATION ; LINKAGE ; LYMPHOMA ; ASSAY ; COUNTRIES ; UNITED-STATES ; vaccination ; time trends ; NON-HODGKINS-LYMPHOMA ; ONCOLOGY ; ASSOCIATIONS ; METAANALYSIS ; biomarker ; NORTHERN
    Abstract: BACKGROUND: Case-control studies suggested a moderate, but consistent association of hepatitis C virus (HCV) infection with lymphoid tissue malignancies, especially non-Hodgkin lymphoma (NHL). More limited data suggested that hepatitis B virus (HBV) infection may also be associated with NHL. However, prospective studies on the topic are few. METHODS: A nested case-control study was performed in eight countries participating in the EPIC prospective study. 739 incident cases of NHL, 238 multiple myeloma (MM), and 46 Hodgkin lymphoma (HL) were matched with 2,028 controls. Seropositivity to anti-HCV, anti-HBc and HBsAg was evaluated and conditional logistic regression was used to estimate odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for NHL, MM or HL, and their combination. RESULTS: Anti-HCV seropositivity among controls in different countries ranged from 0 to 5.3%; HBsAg from 0 to 2.7%; and anti-HBc from 1.9 to 45.9%. Similar non-significant associations were found with seropositivity to HBsAg for NHL (OR=1.78; 95% CI: 0.78-4.04), MM (OR=4.00; 95% CI: 1.00-16.0), and HL (OR=2.00; 95% CI: 0.13-32.0). The association between HBsAg and the combination of NHL, MM and HL (OR=2.21; 95% CI: 1.12-4.33) was similar for cancer diagnosed 〈3 and 〉3 years after blood collection. No association was found between anti-HCV and NHL, MM or HL risk, but the corresponding CIs were very broad. CONCLUSIONS: Chronic HBV infection may increase the risk of lymphoid malignancies among healthy European volunteers.Impact: Treatment directed at control of HBV infection should be evaluated in HBsAg-seropositive patients with lymphoid tissue malignancies.
    Type of Publication: Journal article published
    PubMed ID: 21098651
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  • 6
    Keywords: EXPRESSION ; SURVIVAL ; Germany ; MODEL ; MODELS ; CLASSIFICATION ; DIAGNOSIS ; COHORT ; DEATH ; DISEASE ; MORTALITY ; RISK ; GENE ; GENE-EXPRESSION ; microarray ; PATIENT ; MARKER ; IMPACT ; STAGE ; AMPLIFICATION ; gene expression ; microarrays ; AGE ; MARKERS ; HIGH-RISK ; STRATEGIES ; SPONTANEOUS REGRESSION ; PREDICTION ; INFANTS ; pathology ; CHILDREN ; MICROARRAY ANALYSIS ; neuroblastoma ; ONCOLOGY ; REGRESSION ; overall survival ; INDEPENDENT PROGNOSTIC MARKER ; methods ; PROGNOSTIC MARKER ; PROFILES ; EXPRESSION PROFILES ; RISK STRATIFICATION ; SUBGROUPS ; MYC ; PROFILE ; outcome ; STRATEGY ; CONTRIBUTE ; COHORTS ; COX REGRESSION ; clinical oncology ; STRATIFICATION ; prognostic
    Abstract: Purpose To evaluate the impact of a predefined gene expression - based classifier for clinical risk estimation and cytotoxic treatment decision making in neuroblastoma patients. Patients and Methods Gene expression profiles of 440 internationally collected neuroblastoma specimens were investigated by microarray analysis, 125 of which were examined prospectively. Patients were classified as either favorable or unfavorable by a 144- gene prediction analysis for microarrays (PAM) classifier established previously on a separate set of 77 patients. PAM classification results were compared with those of current prognostic markers and risk estimation strategies. Results The PAM classifier reliably distinguished patients with contrasting clinical courses (favorable [n = 249] and unfavorable [n = 191]; 5- year event free survival [EFS] 0.84 +/- 0.03 v 0.38 +/- 0.04; 5-year overall survival [OS] 0.98 +/- 0.01 v 0.56 +/- 0.05, respectively; both P = .001). Moreover, patients with divergent outcome were robustly discriminated in both German and international cohorts and in prospectively analyzed samples (P = .001 for both EFS and OS for each). In subgroups with clinical low-, intermediate-, and high-risk of death from disease, the PAM predictor significantly separated patients with divergent outcome (low-risk 5-year OS: 1.0 v 0.75 +/- 0.10, P = .001; intermediaterisk: 1.0 v 0.82 +/- 0.08, P = .042; and high-risk: 0.81 +/- 0.08 v 0.43 = 0.05, P=.001). In multivariate Cox regression models based on both EFS and OS, PAM was a significant independent prognostic marker (EFS: hazard ratio [HR], 3.375; 95% CI, 2.075 to 5.492; P=.001; OS: HR, 11.119, 95% CI, 2.487 to 49.701; P=.001). The highest potential clinical impact of the classifier was observed in patients currently considered as non - high- risk (n= 289; 5- year EFS: 0.87= 0.02 v 0.44= 0.07; 5- year OS: 1.0 v 0.80= 0.06; both P=.001). Conclusion Gene expression - based classification using the 144- gene PAM predictor can contribute to improved treatment stratification of neuroblastoma patients
    Type of Publication: Journal article published
    PubMed ID: 20567016
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