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  • 1
    Keywords: CANCER ; EXPRESSION ; Germany ; FOLLOW-UP ; DISEASE ; RISK ; ACTIVATION ; ASSOCIATION ; LYMPHOMA ; AGE ; CIGARETTE-SMOKING ; smoking ; DOSE-RESPONSE ; case-control studies ; TOBACCO ; ALCOHOL ; SMOKERS ; EUROPE ; INTERVIEW ; Hodgkin's lymphoma ; DRINKING ; ONCOLOGY ; case-control study ; RE ; alcohol drinking ; case control studies ; INTERVAL ; NEVER SMOKERS ; odds ratio ; HEMATOLYMPHOPOIETIC MALIGNANCIES ; STERNBERG CELLS
    Abstract: We analysed the effects of tobacco and alcohol in the aetiology of Hodgkin's lymphoma (HL), based on 340 cases and 2465 controls enrolled in Spain, France, Italy, Germany, Ireland and Czech Republic, between 1998 and 2004. Current smokers showed a significantly increased odds ratio (OR) of HL of 1.39 (95% confidence interval (CI) = 1.04-1.87). Analyses were also conducted separately for subjects younger than 35 years (179 cases) and for older subjects (161 cases). For subjects below age 35, no association was observed between tobacco and HL, whereas for older subjects, ever-smokers experienced a doubled risk of HL as compared to never smokers and the OR of HL for current smoking was 2.35 (95% CI = 1.52-3.61), with suggestion of a dose response relationship. A protective effect of alcohol was observed in both age groups. The OR for ever-regular drinking was 0.58 (95% CI = 0.38-0.89) for younger subjects and 0.50 (95% CI = 0.34-0.74) for older subjects. There was no evidence of interaction between tobacco and alcohol. Our results are consistent with previous studies, suggesting a protective effect of alcohol on HL. An effect of tobacco was suggested for HL occurring in middle and late age, although this finding might have occurred by chance
    Type of Publication: Journal article published
    PubMed ID: 16819547
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  • 2
    Keywords: human ; neoplasms ; CLASSIFICATION ; EPIDEMIOLOGY ; NEW-YORK ; RISK ; SAMPLE ; SAMPLES ; INFECTION ; ASSOCIATION ; antibodies ; antibody ; virus ; LYMPHOMA ; ASSAY ; AGE ; LYMPHOCYTES ; case-control studies ; PREVALENCE ; EUROPE ; B-CELL LYMPHOMA ; HUMAN-IMMUNODEFICIENCY-VIRUS ; SERUM ; ADULT ; case-control study ; MALIGNANT-LYMPHOMA ; MIXED CRYOGLOBULINEMIA ; RECIPIENTS ; non-Hodgkin lymphoma ; analysis ; methods ; SUBTYPES ; ASSAYS ; USA ; B-CELL ; MALIGNANT-LYMPHOMAS ; LOW-GRADE ; non Hodgkin lymphoma ; VIRUS CORE PROTEIN ; CONSORTIUM ; red ; INTERLYMPH
    Abstract: Background & Aims: increasing evidence points towards a role of hepatitis C virus (HCV) infection in causing malignant lymphomas. We pooled case-control study data to provide robust estimates of the risk of non-Hodgkin's lymphoma (NHL) subtypes after HCV infection. Methods: The analysis included 7 member studies from the International Lymphoma Epidemiology Consortium (InterLymph) based in Europe, North America, and Australia. Adult cases of NHL (n = 4784) were diagnosed between 1988 and 2004 and controls (n = 6269) were matched by age, sex, and study center. All studies used third-generation enzyme-linked immunosorbent assays to test for antibodies against HCV in serum samples. Participants who were human immunodeficiency virus positive or were organ-transplant recipients were excluded. Results: HCV infection was detected in 172 NHL cases (3.60%) and in 169 (2.70%) controls (odds ratio [OR], 1.78; 95% confidence interval [CI], 1.40 -2.25). In subtype-specific analyses, HCV prevalence was associated with marginal zone lymphoma (OR, 2.47; 95% CI, 1.44-4.23), diffuse large B-cell lymphoma (OR, 2.24; 95% CI, 1.682.99), and lymphoplasmacytic lymphoma (OR, 2.57; 95% CI, 1.14-5.79). Notably, risk estimates were not increased for follicular lymphoma (OR, 1.02; 95% CI, 0.65-1.60). Conclusions: These results confirm the association between HCV infection and NHL and specific B-NHL subtypes (diffuse large B-cell lymphoma, marginal zone lymphoma, and lymphoplasmacytic lymphoma)
    Type of Publication: Journal article published
    PubMed ID: 18387498
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  • 3
    Keywords: SPECTRA ; BLOOD ; neoplasms ; CLASSIFICATION ; GENERATION ; RISK ; RNA ; PATIENT ; INFECTION ; LIVER-TRANSPLANTATION ; ASSOCIATION ; antibodies ; antibody ; virus ; NO ; LYMPHOMA ; MALIGNANCIES ; AGE ; etiology ; LYMPHOCYTES ; case-control studies ; PREVALENCE ; immunosuppression ; B-CELL LYMPHOMA ; HEMOPHILIA ; NON-HODGKINS-LYMPHOMA ; ELISA ; MALIGNANCY ; REGRESSION ; ASSOCIATIONS ; GRADE ; HCV ; hepatitis C ; LYMPHOPROLIFERATIVE DISORDERS ; MALIGNANT-LYMPHOMA ; MIXED CRYOGLOBULINEMIA ; REARRANGEMENT ; RECIPIENTS
    Abstract: Hepatitis C virus (HCV) has been implicated in the etiology of malignant lymphomas. We estimated the risk of lymphoma associated with detection of HCV infection. Cases (n = 529) were consecutive patients newly diagnosed with a lymphoid malignancy between 1998 and 2002 in 4 centers in Spain. Lymphomas were diagnosed and classified using the WHO Classification. Controls (n = 600) were hospitalized patients matched to the cases by 5-year age group, gender and study center. Several medical conditions associated with severe immunosuppression precluded the eligibility of controls. Patients underwent a personal interview and blood sampling. HCV positive subjects were considered those with antibody response to third generation ELISA or detection of HCV RNA with Amplicor 2.0. Cases were systematically tested for HIV antibodies. We used the chi(2) test and unconditional logistic regression to estimate the odds ratio (OR) and 95% confidence interval (95%. Cl) for lymphoma associated with HCV. HCV infection was detected in 40 cases (73%) and 23 (3.8%) control subjects. Six of 16 patients with HIV-related lymphomas and 4 of 8 organ-recipient-related lymphomas were HCV positive. The analysis, excluding HIV-infected subjects and organ recipients, led to a prevalence of HCV of 5.9% among cases and 3.8% among controls. The age-, gender- and center-adjusted OR for all lymphomas was 1.58 (95% Cl = 0.89-2.79). Among all lymphoma categories, HCV was associated with an increased risk of low grade B-cell lymphomas not otherwise specified (NOS) (OR = 35.98, 95% Cl = 4.70-275.4). A 2-fold excess risk associated to HCV was observed for marginal B-cell lymphomas, diffuse large B-cell lymphoma and lymphoma B NOS but the associations were not statistically significant. HCV infection is associated with an increased risk of a broad spectrum of lymphoid neoplasms among non severely immunocompromised subjects in Spain. (C) 2004 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 15185347
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  • 4
    Keywords: CANCER ; MODEL ; neoplasms ; CLASSIFICATION ; SYSTEM ; SYSTEMS ; HISTORY ; RISK ; TUMORS ; FAMILY ; LYMPHOMA ; HEALTH ; AGE ; family history ; COUNTRIES ; DATABASE ; case-control studies ; CHILDREN ; familial cancer ; heredity ; RELATIVES ; non-hodgkin's lymphoma ; Hodgkin's lymphoma ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; FOLLICULAR LYMPHOMA ; MULTIPLE-MYELOMA ; NON-HODGKINS-LYMPHOMA ; case-control study ; AGGREGATION ; FAMILIES ; CLL ; case control studies ; INTERVAL ; familial aggregation ; LYMPHOMAS ; FAMILY-HISTORY ; EUROPEAN COUNTRIES ; INCREASED RISK ; odds ratio ; B-CELL ; TRANSMISSION ; 1ST-DEGREE RELATIVES ; chronic lymphocytic leukaemia
    Abstract: Lymphomas have a potentially important familial component; large studies using recent classification systems are lacking. Based on a multicentre case-control study in seven European countries, we recruited 2480 cases of lymphoid neoplasms (LN) and 2540 controls, matched by country, age and sex. Diagnoses were established according to the World Health Organisation (WHO) classification. We estimated odds ratios (OR) and 95% confidence intervals (CI) for cancer in first-degree relatives and for the kind of relative affected. The OR of LN for a family history of haematological cancer was 1.6 (OR = 1.2-2.1). The OR was particularly high for chronic lymphocytic leukaemia (CLL) (OR = 2.9 [1.9-4.5]). A familial case of lymphoma increased the risk of Hodgkin's lymphoma (HL) (OR = 3.4 [1.5-7.8]). No increased risk was observed for diffuse large B-cell and follicular lymphomas. For CLL and HL, the risk was similar in parents, offspring and siblings. Our study suggests familial aggregation of CLL with a family history of haematological cancer and of HL with a family history of lymphoma. The transmission pattern suggests a dominant model of heredity. (c) 2006 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16928444
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  • 5
    Keywords: CANCER ; EXPRESSION ; Germany ; neoplasms ; DIAGNOSIS ; POPULATION ; RISK ; DISTINCT ; PROTEIN ; PROTEINS ; SAMPLE ; SAMPLES ; PATIENT ; RESPONSES ; INFECTION ; SERA ; ANTIGEN ; ANTIGENS ; T-CELL ; antibodies ; antibody ; ENTRY ; virus ; LYMPHOMA ; MALIGNANCIES ; PATTERNS ; AGE ; COUNTRIES ; DIVERSITY ; CANCER-PATIENTS ; case-control studies ; ANTIBODY-RESPONSES ; EPITOPE ; EPITOPES ; SERIES ; IMBALANCES ; CANCER PATIENTS ; EPSTEIN-BARR-VIRUS ; HODGKINS-DISEASE ; FOLLICULAR LYMPHOMA ; SERUM ; ELISA ; Epstein-Barr virus ; MALIGNANCY ; ONCOLOGY ; DISORDERS ; case control study ; case-control study ; SUBSET ; PATTERN ; BZLF1 ; VIRUS-INFECTION ; EBV INFECTION ; LEVEL ; case control studies ; INTERVAL ; analysis ; EVENTS ; leukaemia ; USA ; LOSSES ; EBV ; EVALUATE ; odds ratio ; RISK-FACTOR ; B-CELL ; case control ; CELL LYMPHOMAS ; Epstein Barr virus ; LATENT INFECTION ; MONONUCLEOSIS
    Abstract: Epstein-Barr Virus (EBV) is consistently associated with distinct lymphoproliferative malignancies and aberrant EBV antibody patterns are found in most EBV cancer patients. We evaluate the detection of an abnormal reactive serological pattern to EBV (ab_EBV) infection and the risk of lymphoma in a multicentric case-control study. Serum samples were collected at study entry from 1,085 incident lymphoma cases from Spain, France, Germany, Czech Republic, Italy and 1,153 age, sex and country matched controls. EBV immunoglobulin G (IgG) serostatus was evaluated through a peptide-based ELISA combining immunodominant epitopes of EBNA1 (BKRF1) and VCA-p18 (BFRF3). Further, immunoblot analysis was performed to evaluate distinct antibody diversity patterns to EBV early antigens (EA), besides EBNA1, VCA-p18, VCA-p40 (BdRF1) and Zebra (BZLF1). Patients with chronic active EBV infection and aberrant EBV activity were characterized as having an abnormal reactive pattern (ab_EBV). Ab EBV was observed in 20.9% of 2,238 included subjects with an increased proportion of cases presenting ab_EBV as compared to the control population (23.9% vs. 18.0% p = 0.001). Ab_EBV positivity was a risk factor for all lymphomas combined (odds ratio [OR] = 1.42, 95% confidence interval [CI]=1.15-1.74), and specifically for chronic lymphocytic leukaemia (OR = 2.96, 95%CI = 2.22-3.95). Lower levels of ab EBV were observed for follicular lymphoma (OR = 0.38, 95%-CI = 0.15-0.98). EBV may be involved in a larger subset of lymphomas among clinically immunocompetent subjects than previously thought, probably explained by an underlying loss of immune control of EBV latent infection. Ab_EBV is a useful too] to explore EBV imbalances preceeding or paralleling possible EBV associated oncogenic events. (C) 2007 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17557295
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  • 6
    Keywords: CANCER ; MODEL ; MODELS ; DIAGNOSIS ; DISEASE ; DISEASES ; HISTORY ; POPULATION ; RISK ; REDUCTION ; SKIN ; ASSOCIATION ; PROGRESSION ; LYMPHOMA ; AGE ; WOMEN ; case-control studies ; INDIVIDUALS ; asthma ; ATOPY ; case control study ; case-control study ; MEDICAL HISTORY ; SAN-FRANCISCO ; allergy ; hay fever ; non-Hodgkin lymphoma ; LEVEL ; pooled analysis ; BIRTH-ORDER ; USA ; CANCER INCIDENCE ; cancer research ; NON-HODGKIN-LYMPHOMA ; FRANCISCO BAY AREA ; HEMATOLOGICAL MALIGNANCIES ; ECZEMA ; CONFIDENCE-INTERVALS ; INTERLYMPH ; ALLERGIES ; CONFIDENCE
    Abstract: We performed a pooled analysis of data on atopic disease and risk of non-Hodgkin lymphoma (NHL) from 13 case-control studies, including 13,535 NHL cases and 16,388 controls. Self-reported atopic diseases diagnosed 2 years or more before NHL diagnosis (cases) or interview (controls) were analyzed. Pooled odds ratios (OR) and 95% confidence intervals (95% CI) were computed in two-stage random-effects or joint fixed-effects models, and adjusted for age, sex, and study center. When modeled individually, lifetime history of asthma, flay fever, specific allergy (excluding hay fever, asthma, and eczema), and food allergy were associated with a significant reduction in NHL, risk, and there was no association for eczema. When each atopic condition was included in the same model, reduced NHL risk was only associated with a history of allergy (OR, 0.80; 95% CI, 0.68-0.94) and reduced R-cell NHL risk was associated with history of hay fever (OR, 0.85; 95% CI, 0.77-0.95) and allergy (OR, 0.84; 95% CI, 0.76-0.93). Significant reductions in B-cell NHL risk were also observed individuals who were likely to be truly or highly atopic-those with hay fever, allergy, or asthma and at least one other atopic condition over their lifetime. The inverse associations were consistent for the diffuse large B-cell and follicular subtypes. Eczema was positively associated with lymphomas of the skin; misdiagnosis of lymphoma as eczema is likely, but progression of eczema to cutaneous lymphoma cannot be excluded. This Pooled study shows evidence of a modest but consistent reduction in the risk of B-cell NHL associated with atopy. [Cancer Res 2009;69(16):6482-9]
    Type of Publication: Journal article published
    PubMed ID: 19654312
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  • 7
    Keywords: Germany ; COHORT ; RISK ; RISK-FACTORS ; ASSOCIATION ; LYMPHOMA ; AGE ; CIGARETTE-SMOKING ; etiology ; MEN ; smoking ; COUNTRIES ; RECRUITMENT ; UNITED-STATES ; case-control studies ; TOBACCO ; ALCOHOL ; CONSUMPTION ; EUROPE ; non-hodgkin's lymphoma ; MULTICENTER ; MULTIPLE-MYELOMA ; OLDER WOMEN ; case-control study ; RE ; case control studies ; SUBTYPES ; pooled analysis ; CANCER-MORTALITY ; MULTICENTER CASE-CONTROL ; non-Hodgkin's
    Abstract: To study the role of tobacco smoking and alcohol drinking in the etiology of non-Hodgkin's lymphoma (NHL), we conducted a multicenter case-control study in Spain, France, Germany, Italy, Ireland and Czech Republic between 1998 and 2004, which included 1,742 cases of NHL and 2,465 controls matched on age, sex and recruitment area. Tobacco smoking was not associated with the risk of NHL overall or with risk of specific histological subtypes. Similarly, there was no association between alcohol drinking and the risk of NHL overall or across histological subtypes. However. a protective effect of alcohol drinking was observed among men (OR = 0.76, 95% CI = 0.62-0.93) and in non-Mediterranean countries (OR = 0.73, 95% CI = 0.61-0.86). There was no evidence of interaction between alcohol drinking and tobacco smoking in NHL etiology. The results of this large-scale European study did not support an association between tobacco and NHL and suggested a protective effect of alcohol on development of NHL for men and in non-Mediterranean countries. (c) 2006 Wiley-Liss. Inc
    Type of Publication: Journal article published
    PubMed ID: 16557575
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  • 8
    Keywords: Germany ; human ; MODEL ; EXPOSURE ; HEPATOCELLULAR-CARCINOMA ; HISTORY ; RISK ; RNA ; INFECTION ; FAMILY ; T cell ; T-CELL ; ASSOCIATION ; POLYMORPHISMS ; virus ; LYMPHOMA ; MALIGNANCIES ; AGE ; family history ; etiology ; COUNTRIES ; leukemia ; PATHOGENESIS ; REPLICATION ; case-control studies ; INDIVIDUALS ; PREVALENCE ; INTERVIEW ; MULTICENTER ; B-CELL LYMPHOMA ; immunoassay ; NON-HODGKINS-LYMPHOMA ; SERUM ; MALIGNANCY ; case-control study ; RE ; FAMILIES ; VIRUS-INFECTION ; LYMPHOPROLIFERATIVE DISORDERS ; MIXED CRYOGLOBULINEMIA ; METAANALYSIS ; case control studies ; INTERVAL ; ENZYME ; SUBTYPES ; LYMPHOMAS ; SIZE ; FAMILY-HISTORY ; EUROPEAN COUNTRIES ; odds ratio ; B-CELL ; EXPOSURES ; MULTICENTER CASE-CONTROL ; RARE ; SAMPLE-SIZE ; HCV INFECTION
    Abstract: Background & Aims: Increasing evidence points toward a role of hepatitis C virus (HCV) infection in the etiology of malignant lymphomas. However, previous epidemiologic studies were limited in size to establish an association between HCV infection and specific lymphoma subtypes. We performed a large, multicenter, case-control study to address this question. Methods: The study comprised 5 European countries and included newly diagnosed cases of any lymphoid malignancy recruited between 1998 and 2004. Controls were matched to cases by 5-year age group, sex, and study center. In-person interviews were conducted to collect data on demographic, medical, and family history as well as environmental exposures. Serum samples of 1807 cases and 1788 controls (excluding human immunodeficiency virus-positive and organ-transplantation subjects) were screened for HCV infection using an enzyme immunoassay. Positive as well as randomly selected negative samples were subjected to HCV RNA detection and HCV genotyping. Results: HCV infection was detected in 53 (2.9%) lymphoma cases and in 41 (2.3%) control subjects (odds ratio [OR], 1.42; 95% confidence interval [CI]: 0.93-2.15). Restricted to individuals who tested positive for HCV-RNA (indicating persistent infection and active viral replication), the OR was 1.82 (95% CI: 1.13-2.91). In subtype-specific analyses, HCV prevalence was associated with diffuse large B-cell lymphoma (OR, 2.19; 95% CI: 1.23-3.91) but not with chronic lymphocytic leukemia or follicular, Hodgkin's, or T-cell lymphoma. The sample size was not sufficient to derive any conclusions for rare lymphoma entities such as splenic marginal zone lymphoma. Conclusions: These results support a model that chronic HCV replication contributes to lymphomagenesis and establish a specific role of HCV infection in the pathogenesis of diffuse large B-cell lymphoma
    Type of Publication: Journal article published
    PubMed ID: 17087949
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  • 9
    Keywords: THERAPY ; PATIENT ; TRIALS ; AGE ; REPRODUCIBILITY ; POSTMENOPAUSAL WOMEN ; REQUIRING PROLONGED OBSERVATION ; RECALL ; COLLABORATIVE REANALYSIS ; SEX-HORMONES
    Abstract: BACKGROUND: Menarche and menopause mark the onset and cessation, respectively, of ovarian activity associated with reproduction, and affect breast cancer risk. Our aim was to assess the strengths of their effects and determine whether they depend on characteristics of the tumours or the affected women. METHODS: Individual data from 117 epidemiological studies, including 118 964 women with invasive breast cancer and 306 091 without the disease, none of whom had used menopausal hormone therapy, were included in the analyses. We calculated adjusted relative risks (RRs) associated with menarche and menopause for breast cancer overall, and by tumour histology and by oestrogen receptor expression. FINDINGS: Breast cancer risk increased by a factor of 1.050 (95% CI 1.044-1.057; p〈0.0001) for every year younger at menarche, and independently by a smaller amount (1.029, 1.025-1.032; p〈0.0001), for every year older at menopause. Premenopausal women had a greater risk of breast cancer than postmenopausal women of an identical age (RR at age 45-54 years 1.43, 1.33-1.52, p〈0.001). All three of these associations were attenuated by increasing adiposity among postmenopausal women, but did not vary materially by women's year of birth, ethnic origin, childbearing history, smoking, alcohol consumption, or hormonal contraceptive use. All three associations were stronger for lobular than for ductal tumours (p〈0.006 for each comparison). The effect of menopause in women of an identical age and trends by age at menopause were stronger for oestrogen receptor-positive disease than for oestrogen receptor-negative disease (p〈0.01 for both comparisons). INTERPRETATION: The effects of menarche and menopause on breast cancer risk might not be acting merely by lengthening women's total number of reproductive years. Endogenous ovarian hormones are more relevant for oestrogen receptor-positive disease than for oestrogen receptor-negative disease and for lobular than for ductal tumours. FUNDING: Cancer Research UK.
    Type of Publication: Journal article published
    PubMed ID: 23084519
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