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  • 1
    Keywords: CANCER ; LUNG ; MODEL ; MODELS ; FOLLOW-UP ; lung cancer ; LUNG-CANCER ; COHORT ; HISTORY ; RISK ; RISKS ; primary ; RISK-FACTORS ; INTERVENTION ; ASSOCIATION ; BREAST-CANCER ; risk factors ; smoking ; cancer risk ; RISK FACTOR ; DATABASE ; DIETARY ; CANCER-RESEARCH ; FRUIT ; QUESTIONNAIRE ; SMOKERS ; EUROPE ; FOOD ; RELATIVE RISK ; BETA-CAROTENE ; FOOD-FREQUENCY QUESTIONNAIRE ; SUPPLEMENT ; CARDIOVASCULAR-DISEASE ; ASSESSMENT INSTRUMENTS ; COMPOSITION DATABASE ; SERUM MICRONUTRIENTS ; VITAMIN-A ; WOMENS-HEALTH ; YORK-STATE COHORT
    Abstract: Intervention trials with supplemental beta-carotene have observed either no effect or a harmful effect on lung cancer risk. Because food composition databases for specific carotenoids have only become available recently, epidemiological evidence relating usual dietary levels of these carotenoids with lung cancer risk is limited. We analyzed the association between lung cancer risk and intakes of specific carotenoids using the primary data from seven cohort studies in North America and Europe. Carotenoid intakes were estimated from dietary questionnaires administered at baseline in each study. We calculated study-specific multivariate relative risks (RRs) and combined these using a random-effects model. The multivariate models included smoking history and other potential risk factors. During follow-up of up to 7-16 years across studies, 3,155 incident lung cancer cases were diagnosed among 399,765 participants. beta-Carotene intake was not associated with lung cancer risk (pooled multivariate RR = 0.98; 95% confidence interval, 0.87-1.11; highest versus lowest quintile). The RRs for alpha-carotene, lutein/zeaxanthin, and lycopene were also close to unity. beta-Cryptoxanthin intake was inversely associated with lung cancer risk (RR = 0.76; 95% confidence interval, 0.67-0.86; highest versus lowest quintile). These results did not change after adjustment for intakes of vitamin C (with or without supplements), folate (with or without supplements), and other carotenoids and multivitamin use. The associations generally were similar among never, past, or current smokers and by histological type. Although smoking is the strongest risk factor for lung cancer, greater intake of foods high in P-cryptoxanthin, such as citrus fruit, may modestly lower the risk
    Type of Publication: Journal article published
    PubMed ID: 14744731
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  • 2
    Keywords: CANCER ; MODEL ; CLASSIFICATION ; DIAGNOSIS ; EPIDEMIOLOGY ; MORTALITY ; RISK ; ASSOCIATION ; WOMEN ; case-control studies ; ALCOHOL-CONSUMPTION ; QUESTIONNAIRE ; EUROPE ; SKIN-CANCER ; SUNLIGHT ; CELL CARCINOMA ; pooled analysis ; B-CELL ; VITAMIN-D ; non Hodgkin lymphoma ; personal sun exposure ; ULTRAVIOLET-RADIATION EXPOSURE
    Abstract: In 2004-2007 4 independent case-control studies reported evidence that sun exposure might protect against NHL; a fifth, in women only, found increased risks of NHL associated with a range of sun exposure measurements. These 5 studies are the first to examine the association between personal sun exposure and NHL. We report here on the relationship between sun exposure and NHL in a pooled analysis of 10 studies participating in the International Lymphoma Epidemiology Consortium (InterLymph), including the 5 published studies. Ten case-control studies covering 8,243 cases and 9,697 controls in the USA, Europe and Australia contributed original data for participants of European origin to the pooled analysis. Four kinds of measures of self-reported personal sun exposure were assessed at interview. A two-stage estimation method was used in which study-specific odds ratios (ORs) and 95% confidence intervals (CIs), adjusted for potential confounders including smoking and alcohol use, were obtained from unconditional logistic regression models and combined in random-effects models to obtain the pooled estimates. Risk of NHL fell significantly with the composite measure of increasing recreational sun exposure, pooled OR = 0.76 (95% CI 0.63-0.91) for the highest exposure category (p for trend 0.01). A downtrend in risk with increasing total sun exposure was not statistically significant. The protective effect of recreational sun exposure was statistically significant at 18-40 years of age and in the 10 years before diagnosis, and for B cell, but not T cell, lymphomas. Increased recreational sun exposure may protect against NHL. (C) 2007 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17708556
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  • 3
  • 4
    Keywords: CANCER ; neoplasms ; POLYMORPHISMS ; UNITED-STATES ; ALCOHOL-CONSUMPTION ; SAN-FRANCISCO ; AGGREGATION ; FRANCISCO BAY AREA ; CONNECTICUT WOMEN ; MIGRANTS
    Abstract: A role for genetic susceptibility in non-Hodgkin lymphoma (NHL) is supported by the accumulating evidence of common genetic variations altering NHL risk. However, the pattern of NHL heritability remains poorly understood. We conducted a pooled analysis of 10 211 NHL cases and 11905 controls from the International Lymphoma Epidemiology Consortium (InterLymph) to evaluate NHL risk among those with hematopoietic malignancies in first-degree relatives. Odds ratios (ORs) and 95% confidence intervals (CIs) of NHL and its subtypes were estimated from unconditional logistic regression models with adjustment for confounders. NHL risk was elevated for individuals who reported first-degree relatives with NHL (OR = 1.5; 95% CI = 1.2-1.9), Hodgkin lymphoma (OR = 1.6; 95% Cl = 1.1-2.3), and leukemia (OR = 1.4; 95% CI = 1.2-2.7). Risk was highest among individuals who reported a brother with NHL (OR = 2.8; 95% CI = 1.6-4.8) and was consistent for all NHL subtypes evaluated. If a first-degree relative had Hodgkin lymphoma, NHL risk was highest if the relative was a parent (OR = 1.7; 95% CI = 1.0-2.9). If a first-degree relative had leukemia, NHL risk was highest among women who reported a sister with leukemia (OR = 3.0; 95% CI = 1.6-5.6). The pattern of NHL heritability appeared to be uniform across NHL subtypes, but risk patterns differed by specific hematopoietic malignancies and the sex of the relative, revealing critical clues to disease etiology.
    Type of Publication: Journal article published
    PubMed ID: 17185468
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  • 5
    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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  • 6
    Abstract: An RNAi-based functional screening of mitotic kinases in Drosophila recently identified a number of members of the kinome that are required for normal cell division. Depletion of these kinases resulted in a number of different mitotic abnormalities including spindle malformation, chromosome mis-segregation, centrosome amplification and failure of cytokinesis (Bettencourt-Dias et al. in Nature 432:980-987, 2004). Since mitotic defects are commonly observed in cancer cells, these kinases may contribute to tumor development and/or progression. To investigate whether common genetic variation in the mitotic kinases are associated with breast cancer risk, we genotyped 386 single nucleotide polymorphisms (SNPs) from 44 mitotic kinase genes, in 798 breast cancer cases and 843 unaffected controls from a clinic-based study. A total of 22 SNPs from 13 kinase genes displayed significant associations with breast cancer risk (P(trend) 〈 or = 0.05), including two SNPs from FYN (rs6914091 and rs1465061) that remained of interest after accounting for multiple testing (q = 0.06). These associations were stronger when evaluating cases with estrogen and progesterone receptor positive tumors. In addition, haplotype-based tests identified significant associations with risk for common haplotypes of the MAST2 (P = 0.04) and MAP2K4 (P = 0.006) genes. Although requiring replication, these findings suggest that genetic polymorphisms in mitotic kinases that have been implicated in chromosome instability and aneuploidy may contribute to the development of breast cancer.
    Type of Publication: Journal article published
    PubMed ID: 19404734
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  • 7
    Keywords: CANCER ; human ; PATHWAY ; PATHWAYS ; DISEASE ; EPIDEMIOLOGY ; POPULATION ; RISK ; GENE ; GENES ; TUMOR-NECROSIS-FACTOR ; ASSOCIATION ; polymorphism ; SUSCEPTIBILITY ; LYMPHOMA ; case-control studies ; INDIVIDUALS ; ALCOHOL-CONSUMPTION ; B-CELL LYMPHOMA ; FACTOR-ALPHA ; CYTOKINE ; case-control study ; case control studies ; single-nucleotide ; single-nucleotide polymorphism ; GENOTYPE DATA ; pooled analysis ; INTERLEUKIN-10 ; PROMOTER POLYMORPHISMS ; BIOLOGICAL IMPLICATIONS
    Abstract: Background Common genetic variants in immune and inflammatory response genes can affect the risk of developing non-Hodgkin lymphoma. We aimed to test this hypothesis using previously unpublished data from eight European, Canadian, and US case-control studies of the International Lymphoma Epidemiology Consortium (InterLymph). Methods We selected 12 single-nucleotide polymorphisms for analysis, on the basis of previous functional or association data, in nine genes that have important roles in lymphoid development, Th1/Th2 balance, and proinflammatory or anti-inflammatory pathways (IL1A, IL1RN, IL1B, IL2, IL6, IL10, TNF, LTA, and CARD15). Genotype data for one or more single-nucleotide polymorphisms were available for 3586 cases of non-Hodgkin lymphoma and for 4018 controls, and were assessed in a pooled analysis by use of a random-effects logistic regression model. Findings The tumour necrosis factor (TNF) -308G -〉 A polymorphism was associated with increased risk of nonHodgkin lymphoma (p for trend=0 . 005), particularly for diffuse large B-cell lymphoma, the main histological subtype (odds ratio 1 . 29 [95% CI 1 . 10-1 . 51] for GA and 1.65 [1 . 16-2 . 34] for AA, p for trend 〈 0 . 0001), but not for follicular lymphoma. The interleukin 10 (IL10) -3575T -〉 A polymorphism was also associated with increased risk of non-Hodgkin lymphoma (p for trend=0 . 02), again particularly for diffuse large B-cell lymphoma (p for trend=0 . 006). For individuals homozygous for the TNF -308A allele and carrying at least one IL 10 -3575A allele, risk of diffuse large B-cell lymphoma doubled (2 . 13 [1 . 37-3 . 32], p=0 . 00083). Interpretation Common polymorphisms in TNF and IL10, key cytokines for the inflammatory response and Th1/Th2 balance, could be susceptibility loci for non-Hodgkin lymphoma. Moreover, our results underscore the importance of consortia for investigating the genetic basis of chronic diseases like cancer
    Type of Publication: Journal article published
    PubMed ID: 16389181
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  • 8
    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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  • 9
    Keywords: RISK ; COMPLEX ; COMPLEXES ; ASSOCIATION ; POLYMORPHISMS ; SUSCEPTIBILITY ; VARIANTS ; LYMPHOMA ; genetics ; HLA ; FOLLICULAR LYMPHOMA ; VARIANT ; HIGH-RESOLUTION ; non-Hodgkin lymphoma ; SUBTYPES ; HAPLOTYPE ; LOCUS ; LOCI ; susceptibility loci ; NON-HODGKIN-LYMPHOMA ; GENOME-WIDE ASSOCIATION ; GENETIC-VARIATION ; non-Hodgkin ; Genetic ; NECROSIS-FACTOR TNF
    Abstract: To identify susceptibility loci for non-Hodgkin lymphoma subtypes, we conducted a three-stage genome-wide association study. We identified two variants associated with follicular lymphoma at 6p21.32 (rs10484561, combined P = 1.12 x 10(-29) and rs7755224, combined P = 2.00 x 10(-19); r(2) = 1.0), supporting the idea that major histocompatibility complex genetic variation influences follicular lymphoma susceptibility. We also found confirmatory evidence of a previously reported association between chronic lymphocytic leukemia/small lymphocytic lymphoma and rs735665 (combined P = 4.24 x 10(-9))
    Type of Publication: Journal article published
    PubMed ID: 20639881
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  • 10
    Keywords: BLOOD ; MODEL ; DISEASE ; RISK ; PATIENT ; ARTHRITIS ; RISK-FACTORS ; T cell ; T-CELL ; TYPE-1 ; ASSOCIATION ; DISORDER ; LYMPHOMA ; risk factors ; SWEDEN ; diabetes ; case-control studies ; CLUES ; MULTIPLE-SCLEROSIS ; FOLLICULAR LYMPHOMA ; INFLAMMATORY-BOWEL-DISEASE ; SYSTEMIC-LUPUS-ERYTHEMATOSUS ; DISORDERS ; case-control study ; MEDICAL HISTORY ; POPULATION-BASED COHORT ; PATTERN ; T-CELL LYMPHOMA ; rheumatoid arthritis ; RHEUMATOID-ARTHRITIS ; non-Hodgkin lymphoma ; analysis ; SUBTYPES ; CELIAC-DISEASE ; PARTICIPANTS ; multiple sclerosis ; pooled analysis ; USA ; CANCER INCIDENCE ; RISK-FACTOR ; B-CELL ; ANEMIA ; PERNICIOUS-ANEMIA ; systemic ; RATIO ; non Hodgkin lymphoma ; POOLED-ANALYSIS ; non-Hodgkin ; CONSORTIUM ; CONFIDENCE-INTERVALS ; MARGINAL ZONE LYMPHOMAS ; INTERLYMPH ; AUTOIMMUNE ; HEMATOPOIETIC CANCER ; hemolytic anemia ; PRIMARY SJOGRENS-SYNDROME ; systemic lupus erythematosus
    Abstract: Some autoimmune disorders are increasingly recognized as risk factors for non-Hodgkin lymphoma (NHL) overall, but large-scale systematic assessments of risk of NHL subtypes are lacking. We performed a pooled analysis of self-reported autoimmune conditions and risk of NHL and subtypes, including 29 423 participants in 12 case-control studies. We computed pooled odds ratios (OR) and 95% confidence intervals (CI) in a joint fixed-effects model. Sjogren syndrome was associated with a 6.5-fold increased risk of NHL, a 1000-fold increased risk of parotid gland marginal zone lymphoma (OR = 996; 95% CI, 216-4596), and with diffuse large B-cell and follicular lymphomas. Systemic lupus erythematosus was associated with a 2.7-fold increased risk of NHL and with diffuse large B-cell and marginal zone lymphomas. Hemolytic anemia was associated with diffuse large B-cell NHL. T-cell NHL risk was increased for patients with celiac disease and psoriasis. Results for rheumatoid arthritis were heterogeneous between studies. Inflammatory bowel disorders, type 1 diabetes, sarcoidosis, pernicious anemia, and multiple sclerosis were not associated with risk of NHL or subtypes. Thus, specific autoimmune disorders are associated with NHL risk beyond the development of rare NHL subtypes in affected organs. The pattern of associations with NHL subtypes may harbor clues to lymphomagenesis
    Type of Publication: Journal article published
    PubMed ID: 18263783
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