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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 ; EXPRESSION ; GROWTH ; tumor ; CELL ; MODEL ; PATHWAY ; PATHWAYS ; COHORT ; DISEASE ; GENE ; GENE-EXPRESSION ; RNA ; DIFFERENTIATION ; TUMORS ; ACTIVATION ; BINDING ; BIOLOGY ; TARGET ; CHROMATIN ; gene expression ; PROMOTER ; genetics ; MODULATION ; C-MYC ; REPRESSION ; TRANSCRIPTIONAL REPRESSION ; MYCN ; neuroblastoma ; N-MYC ; signaling ; ONCOLOGY ; B-CELL LYMPHOMAS ; miRNA ; outcome ; MICRORNA ; CELL BIOLOGY ; Genetic ; COHORTS ; EXPRESSION SIGNATURES ; PATHWAY DEREGULATION
    Abstract: Increased activity of MYC protein-family members is a common feature in many cancers. Using neuroblastoma as a tumor model, we established a microRNA (miRNA) signature for activated MYCN/c-MYC signaling in two independent primary neuroblastoma tumor cohorts and provide evidence that c-MYC and MYCN have overlapping functions. On the basis of an integrated approach including miRNA and messenger RNA (mRNA) gene expression data we show that miRNA activation contributes to widespread mRNA repression, both in c-MYC- and MYCN-activated tumors. c-MYC/MYCN-induced miRNA activation was shown to be dependent on c-MYC/MYCN promoter binding as evidenced by chromatin immunoprecipitation. Finally, we show that pathways, repressed through c-MYC/MYCN miRNA activation, are highly correlated to tumor aggressiveness and are conserved across different tumor entities suggesting that c-MYC/MYCN activate a core set of miRNAs for cooperative repression of common transcriptional programs related to disease aggressiveness. Our results uncover a widespread correlation between miRNA activation and c-MYC/MYCN-mediated coding gene expression modulation and further substantiate the overlapping functions of c-MYC and MYCN in the process of tumorigenesis. Oncogene (2010) 29, 1394-1404; doi:10.1038/onc.2009.429; published online 30 November 2009
    Type of Publication: Journal article published
    PubMed ID: 19946337
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  • 5
    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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  • 6
    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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  • 7
    Keywords: CANCER ; EXPRESSION ; RISK ; MARKERS ; SERUM-LEVELS ; NON-HODGKIN-LYMPHOMA ; B-CELL LYMPHOCYTOSIS ; IMMUNE ACTIVATION ; SCD23 ; MBL
    Abstract: BACKGROUND: Chronic lymphocytic leukemia (CLL) is a chronic disease that often progresses slowly from a precursor stage, monoclonal B-cell lymphocytosis (MBL), and that can remain undiagnosed for a long time. METHODS: Within the European Prospective Investigation into Cancer cohort, we measured prediagnostic plasma sCD23 for 179 individuals who eventually were diagnosed with CLL and an equal number of matched control subjects who remained free of cancer. RESULTS: In a very large proportion of CLL patients' plasma sCD23 was clearly elevated 7 or more years before diagnosis. Considering sCD23 as a disease predictor, the area under the ROC curve (AUROC) was 0.95 [95% confidence interval (CI), 0.90-1.00] for CLL diagnosed within 0.1 to 2.7 years after blood measurement, 0.90 (95% CI, 0.86-0.95) for diagnosis within 2.8 to 7.3 years, and 0.76 (95% CI, 0.65-0.86) for CLL diagnosed between 7.4 and 12.5 years. Even at a 7.4-year and longer time interval, elevated plasma sCD23 could predict a later clinical diagnosis of CLL with 100% specificity at 〉45% sensitivity. CONCLUSIONS: Our findings provide unique documentation for the very long latency times during which measurable B-cell lymphoproliferative disorder exists before the clinical manifestation of CLL. IMPACT: Our findings have relevance for the interpretation of prospective epidemiologic studies on the causes of CLL in terms of reverse causation bias. The lag times indicate a time frame within which an early detection of CLL would be theoretically possible. Cancer Epidemiol Biomarkers Prev; 24(3); 538-45. (c)2014 AACR.
    Type of Publication: Journal article published
    PubMed ID: 25542829
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  • 8
    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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  • 9
    Keywords: RECEPTOR ; CANCER ; POPULATION ; RISK ; SITE ; DISTINCT ; GENE ; GENES ; GENOME ; RESOLUTION ; BINDING ; SEQUENCE ; ASSOCIATION ; SUSCEPTIBILITY ; SUSCEPTIBILITY LOCUS ; ALPHA ; BREAST ; breast cancer ; BREAST-CANCER ; genetics ; SNP ; POPULATIONS ; PROJECT ; ESTROGEN-RECEPTOR ; HETEROGENEITY ; ORIGIN ; TAMOXIFEN ; ASSOCIATIONS ; SNPs ; SCIENCE ; ESTROGEN ; HAPLOTYPE ; LOCUS ; TRAITS ; estrogen receptor ; BINDING-SITE ; CHINESE POPULATION ; GENOME-WIDE ASSOCIATION ; AFRICAN-AMERICAN ; ESTROGEN-RECEPTOR-ALPHA ; CONFER SUSCEPTIBILITY ; BINDING SITE ; Genetic ; COMMON VARIANTS ; ANCESTRY ; PANEL ; CAUSAL VARIANTS
    Abstract: We used an approach that we term ancestry-shift refinement mapping to investigate an association, originally discovered in a GWAS of a Chinese population, between rs2046210[T] and breast cancer susceptibility. The locus is on 6q25.1 in proximity to the C6orf97 and estrogen receptor alpha (ESR1) genes. We identified a panel of SNPs that are correlated with rs2046210 in Chinese, but not necessarily so in other ancestral populations, and genotyped them in breast cancer case: control samples of Asian, European, and African origin, a total of 10,176 cases and 13,286 controls. We found that rs2046210[T] does not confer substantial risk of breast cancer in Europeans and Africans (OR = 1.04, P = 0.099, and OR = 0.98, P = 0.77, respectively). Rather, in those ancestries, an association signal arises from a group of less common SNPs typified by rs9397435. The rs9397435[G] allele was found to confer risk of breast cancer in European (OR = 1.15, P = 1.2x10(-3)), African (OR = 1.35, P = 0.014), and Asian (OR = 1.23, P = 2.9x10(-4)) population samples. Combined over all ancestries, the OR was 1.19 (P = 3.9x10(-7)), was without significant heterogeneity between ancestries (P-het = 0.36) and the SNP fully accounted for the association signal in each ancestry. Haplotypes bearing rs9397435[G] are well tagged by rs2046210[ T] only in Asians. The rs9397435[G] allele showed associations with both estrogen receptor positive and estrogen receptor negative breast cancer. Using early-draft data from the 1,000 Genomes project, we found that the risk allele of a novel SNP (rs77275268), which is closely correlated with rs9397435, disrupts a partially methylated CpG sequence within a known CTCF binding site. These studies demonstrate that shifting the analysis among ancestral populations can provide valuable resolution in association mapping
    Type of Publication: Journal article published
    PubMed ID: 20661439
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  • 10
    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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