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  • ASSOCIATION  (12)
  • CHRONIC LYMPHOCYTIC-LEUKEMIA  (6)
  • MORTALITY  (6)
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  • 1
    Keywords: CANCER ; CELLS ; AGENTS ; CELL ; MODEL ; MODELS ; neoplasms ; FOLLOW-UP ; SYSTEM ; COHORT ; cohort study ; EPIDEMIOLOGY ; HISTORY ; incidence ; RISK ; INFECTION ; MECHANISM ; primary ; RISK-FACTORS ; mechanisms ; T cell ; T-CELL ; ASSOCIATION ; DISORDER ; SUSCEPTIBILITY ; NO ; LYMPHOMA ; CARE ; DESIGN ; PLASMA ; AGE ; WOMEN ; etiology ; MEN ; risk factors ; leukemia ; Jun ; diabetes ; ABNORMALITIES ; INFECTIONS ; EPIC ; nutrition ; immunosuppression ; non-hodgkin's lymphoma ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; MULTIPLE-MYELOMA ; VIRAL-INFECTION ; insulin ; MELLITUS ; AGENT ; AUTOIMMUNITY ; multiple myeloma ; DISORDERS ; MEDICAL HISTORY ; INCREASE ; T-CELL LYMPHOMA ; prospective studies ; methods ; SUBTYPES ; metabolic syndrome ; BODY-MASS INDEX ; prospective ; prospective study ; RISK-FACTOR ; CANCERS ; B-CELL ; ENGLAND ; ENVIRONMENTAL-FACTORS ; host ; INCREASES ; viral ; European Prospective Investigation into Cancer ; non-Hodgkin ; neoplasm ; INTERLEUKIN-6 GENE
    Abstract: Background Non-Hodgkin's lymphomas are a heterogeneous group of neoplasms arising from the lymphopoietic system including a wide range of subtypes of either B-cell or T-cell lymphomas. The few established risk factors for the development of these neoplasms include viral infections and immunological abnormalities, but their etiology remains largely unknown. Evidence suggests that certain medical conditions may be linked, through immunosuppression, to the risk of non-Hodgkin's lymphoma. Multiple myeloma is a neoplasm of plasma cells that accounts for approximately 15% of lymphopoietic cancers. Increases in the incidence of non-Hodgkin's lymphoma and multiple myeloma in the past implicate environmental factors as potential causal agents. Design and Methods In the European Prospective Investigation into Cancer and Nutrition (EPIC), 1,213 histologically confirmed incident cases of non-Hodgkin's lymphoma and multiple myeloma (594 men; 619 women) were identified during a follow-up of 8.5 years. Cox proportional hazard models were used to explore the association between self-reported diabetes, diagnosed after 30 years of age, and the risk of non-Hodgkin's lymphoma overall and multiple myeloma and various lymphoma subtypes. Results We found no association between a personal history of diabetes and the risk of non-Hodgkin's lymphoma overall in men (HR: 1.28, 95% CI: 0.89-1.84), in women (HR: 0.71, 95% CI: 0.41-1.24), or in men and women combined (HR: 1.09, 95% CI: 0.80-1.47). Among the B-non-Hodgkin's lymphoma subtypes, we observed a statistically significant increased risk of B-cell chronic lymphocytic leukemia (HR: 2.0, 95% CI: 1.04-3.86) in men, but not in women (HR: 1.07, 95% CI: 0.33-3.43). Conclusions This prospective study did not provide evidence for a role of self-reported diabetes in the etiology of non-Hodgkin's lymphoma overall or multiple myeloma. We found an increased risk of B-cell chronic lymphocytic leukemia among men with diabetes, but not among women. We hypothesize that diabetes may not play a causal role in the etiology of B-cell chronic lymphocytic leukemia, though the underlying pathogenic mechanisms of both disorders may include shared genetic, host and/or environmental susceptibility factors
    Type of Publication: Journal article published
    PubMed ID: 18443270
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  • 2
    Keywords: RECEPTOR ; CANCER ; EXPRESSION ; SURVIVAL ; tumor ; carcinoma ; CELL ; PATHWAYS ; CLASSIFICATION ; DIAGNOSIS ; GENE ; GENE-EXPRESSION ; RNA ; SAMPLE ; SAMPLES ; TUMORS ; PATIENT ; NF-KAPPA-B ; INDEX ; DOWN-REGULATION ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; PROGRESSION ; gene expression ; DESIGN ; AGE ; METASTASIS ; PHENOTYPE ; CANCER-PATIENTS ; CARCINOMAS ; experimental design ; BEHAVIOR ; CANCER PATIENTS ; ESTROGEN-RECEPTOR ; ONCOLOGY ; RE ; GRADE ; ESTROGEN ; analysis ; SUBTYPES ; CHIP ; SIGNATURE ; USA ; cancer research ; VARIABLES ; MOTILITY ; NOV ; aggressiveness ; PROFILE ; response ; CELL MOTILITY ; expression profile ; neoplasm ; POOR SURVIVAL ; HISTOLOGIC GRADE ; SIGNATURES
    Abstract: Purpose: We hypothesize that a gene expression profile characteristic for inflammatory breast cancer (IBC), an aggressive form of breast cancer associated with rapid cancer dissemination and poor survival, might be related to tumor aggressiveness in non-IBC (nIBC). Experimental Design: RNA from 17 IBC samples and 40 nIBC samples was hybridized onto Affymetrix chips. A gene signature predictive of IBC was identified and applied onto 1,157 nIBC samples with survival data of 881 nIBC samples. Samples were classified as IBC-like or nIBC-like. The IBC signature classification was compared with the classifications according to other prognostically relevant gene signatures and clinicopathologic variables. In addition, relapse-free survival (RFS) was compared by the Kaplan-Meyer method. Results: Classification according to the IBC signature is significantly (P 〈 0.05) associated with the cell-of-origin subtypes, the wound healing response, the invasive gene signature, the genomic grade index, the fibroblastic neoplasm signature, and the 70-gene prognostic signature. Significant associations (P 〈 0.01) were found between the IBC signature and tumor grade, estrogen receptor status, ErbB2 status, and patient age at diagnosis. Patients with an IBC-like phenotype show a significantly shorter RFS interval (P 〈 0.05). Oncomine analysis identified cell motility as an important concept linked with the IBC signature. Conclusions:We show that nIBC carcinomas having an IBC-like phenotype have a reduced RFS interval. This suggests that IBC and nIBC show comparable phenotypic traits, for example augmented cell motility, with respect to aggressive tumor cell behavior. This observation lends credit to the use of IBC to study aggressive tumor cell behavior
    Type of Publication: Journal article published
    PubMed ID: 19010862
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  • 3
    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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  • 4
    Keywords: CANCER ; MODEL ; cohort study ; DESIGN ; OBESITY ; UNITED-STATES ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; MULTIPLE-MYELOMA ; physical activity ; multiple myeloma ; non-Hodgkin lymphoma ; EPIDEMIOLOGIC EVIDENCE ; BODY-MASS INDEX ; RISK-FACTOR ; HODGKIN LYMPHOMA ; ACTIVITY QUESTIONNAIRE ; NON-HODGKIN-LYMPHOMA ; ANTHROPOMETRIC CHARACTERISTICS ; Lymphocytic leukaemia ; Lymphoid neoplasm
    Abstract: Background: Lymphoid neoplasms are a heterogeneous group of cancers that originate in the lymphatic cells of the immune system. Several risk factors have been identified or suggested, but they all account for only a small proportion of the lymphoid neoplasm incidence. It has been hypothesised that regular exercise may modulate the immune system and thereby reduce the risk of developing the disease. Design and methods: The European Investigation into Cancer and Nutrition (EPIC) cohort consists of 521,457 adults, recruited by 23 centres in 10 European countries. The analytical cohort included 343,756 participants, with 778 non-Hodgkin lymphoma (NHL) cases (376 men and 402 women) and 690 B-cell non-Hodgkin lymphoma (B-NHL) cases (326 men and 364 women). Multivariate Cox regression models were used to calculate hazard ratios (HR) for the association between total, recreational, occupational, and household physical activity and NHL and B-NHL risk, as well as the risk for several B-NHL subtypes. Models were stratified by study centre and age at recruitment and adjusted for various potential confounding factors. Results: We found no evidence of any effect of total physical activity on NHL (adjusted p-trend = 0.76 and 0.30 for men and women, respectively) and B-NHL risk (adjusted p-trend = 0.99 and 0.21 for men and women, respectively) for either men or women. Also no robust results were found for B-NHL subtype analyses among men or women. Conclusions: This study provided no consistent evidence for an association between various physical activity measures and the risk of lymphoid neoplasms or any of the B-NHL subtypes.
    Type of Publication: Journal article published
    PubMed ID: 21159506
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  • 5
    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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  • 6
    Keywords: TUMORS ; ASSOCIATION ; WOMEN ; ORAL-CONTRACEPTIVES ; HISTOLOGIC TYPE ; LIFE-STYLE FACTORS ; inflammation ; TOBACCO USE ; HORMONE-THERAPY ; BORDERLINE
    Abstract: PURPOSE: The majority of previous studies have observed an increased risk of mucinous ovarian tumors associated with cigarette smoking, but the association with other histological types is unclear. In a large pooled analysis, we examined the risk of epithelial ovarian cancer associated with multiple measures of cigarette smoking with a focus on characterizing risks according to tumor behavior and histology. METHODS: We used data from 21 case-control studies of ovarian cancer (19,066 controls, 11,972 invasive and 2,752 borderline cases). Study-specific odds ratios (OR) and 95 % confidence intervals (CI) were obtained from logistic regression models and combined into a pooled odds ratio using a random effects model. RESULTS: Current cigarette smoking increased the risk of invasive mucinous (OR = 1.31; 95 % CI: 1.03-1.65) and borderline mucinous ovarian tumors (OR = 1.83; 95 % CI: 1.39-2.41), while former smoking increased the risk of borderline serous ovarian tumors (OR = 1.30; 95 % CI: 1.12-1.50). For these histological types, consistent dose-response associations were observed. No convincing associations between smoking and risk of invasive serous and endometrioid ovarian cancer were observed, while our results provided some evidence of a decreased risk of invasive clear cell ovarian cancer. CONCLUSIONS: Our results revealed marked differences in the risk profiles of histological types of ovarian cancer with regard to cigarette smoking, although the magnitude of the observed associations was modest. Our findings, which may reflect different etiologies of the histological types, add to the fact that ovarian cancer is a heterogeneous disease.
    Type of Publication: Journal article published
    PubMed ID: 23456270
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  • 7
    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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  • 8
    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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  • 9
    Keywords: PROGENITOR CELLS ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; NON-HODGKIN-LYMPHOMA ; SOMATIC MUTATIONS ; MONOCLONAL GAMMOPATHY ; B-CELL LYMPHOCYTOSIS ; HEALTHY-INDIVIDUALS ; UNDETERMINED SIGNIFICANCE MGUS ; SMOLDERING MULTIPLE-MYELOMA ; LOW-TUMOR-BURDEN
    Abstract: PURPOSE: The (14;18) translocation constitutes both a genetic hallmark and critical early event in the natural history of follicular lymphoma (FL). However, t(14;18) is also detectable in the blood of otherwise healthy persons, and its relationship with progression to disease remains unclear. Here we sought to determine whether t(14;18)-positive cells in healthy individuals represent tumor precursors and whether their detection could be used as an early predictor for FL. PARTICIPANTS AND METHODS: Among 520,000 healthy participants enrolled onto the EPIC (European Prospective Investigation Into Cancer and Nutrition) cohort, we identified 100 who developed FL 2 to 161 months after enrollment. Prediagnostic blood from these and 218 controls were screened for t(14;18) using sensitive polymerase chain reaction-based assays. Results were subsequently validated in an independent cohort (65 case participants; 128 controls). Clonal relationships between t(14;18) cells and FL were also assessed by molecular backtracking of paired prediagnostic blood and tumor samples. RESULTS: Clonal analysis of t(14;18) junctions in paired prediagnostic blood versus tumor samples demonstrated that progression to FL occurred from t(14;18)-positive committed precursors. Furthermore, healthy participants at enrollment who developed FL up to 15 years later showed a markedly higher t(14;18) prevalence and frequency than controls (P 〈 .001). Altogether, we estimated a 23-fold higher risk of subsequent FL in blood samples associated with a frequency 〉 10(-4) (odds ratio, 23.17; 95% CI, 9.98 to 67.31; P 〈 .001). Remarkably, risk estimates remained high and significant up to 15 years before diagnosis. CONCLUSION: High t(14;18) frequency in blood from healthy individuals defines the first predictive biomarker for FL, effective years before diagnosis.
    Type of Publication: Journal article published
    PubMed ID: 24687831
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  • 10
    Keywords: CANCER ; POPULATION ; RISK ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; FOLLICULAR LYMPHOMA ; TUMORIGENESIS ; NON-HODGKIN-LYMPHOMA ; COMMON VARIANTS ; NECROSIS-FACTOR TNF ; RAL GTPASES
    Abstract: Diffuse large B cell lymphoma (DLBCL) is the most common lymphoma subtype and is clinically aggressive. To identify genetic susceptibility loci for DLBCL, we conducted a meta-analysis of 3 new genome-wide association studies (GWAS) and 1 previous scan, totaling 3,857 cases and 7,666 controls of European ancestry, with additional genotyping of 9 promising SNPs in 1,359 cases and 4,557 controls. In our multi-stage analysis, five independent SNPs in four loci achieved genome-wide significance marked by rs116446171 at 6p25.3 (EXOC2; P = 2.33 x 10-21), rs2523607 at 6p21.33 (HLA-B; P = 2.40 x 10-10), rs79480871 at 2p23.3 (NCOA1; P = 4.23 x 10-8) and two independent SNPs, rs13255292 and rs4733601, at 8q24.21 (PVT1; P = 9.98 x 10-13 and 3.63 x 10-11, respectively). These data provide substantial new evidence for genetic susceptibility to this B cell malignancy and point to pathways involved in immune recognition and immune function in the pathogenesis of DLBCL.
    Type of Publication: Journal article published
    PubMed ID: 25261932
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