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  • 1
    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 We aimed to test this hypothesis using previously unpublished data from eight European, Canadian, and US case-control studies of the International Lymphoma Epidemiology Consortium (InterLymph).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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  • 2
    Keywords: RISK ; GENE ; GENES ; ASSOCIATION ; polymorphism ; SUSCEPTIBILITY ; LYMPHOMA ; PROMOTER ; meta-analysis ; FOLLICULAR LYMPHOMA ; SYSTEMIC-LUPUS-ERYTHEMATOSUS ; VARIANT ; RHEUMATOID-ARTHRITIS ; ALLELES ; pooled analysis ; B-CELL ; SUBGROUPS ; INTERLEUKIN-10 ; SUN EXPOSURE ; GENETIC-VARIATION ; non-Hodgkin ; Genetic ; IMMUNE ; single nucleotide ; lymphotoxin-alpha ; tumor necrosis factor-alpha
    Abstract: In an International Lymphoma Epidemiology Consortium pooled analysis, polymorphisms in 2 immune-system-related genes, tumor necrosis factor (TNF) and interleukin-10 (IL10), were associated with non-Hodgkin lymphoma (NHL) risk. Here, 8,847 participants were added to previous data (patients diagnosed from 1989 to 2005 in 14 case-control studies; 7,999 cases, 8,452 controls) for testing of polymorphisms in the TNF -308G 〉 A (rs1800629), lymphotoxin-alpha (LTA) 252A 〉 G (rs909253), IL10 -3575T 〉 A (rs1800890, rs1800896), and nucleotide-binding oligomerization domain containing 2 (NOD2) 3020insC (rs2066847) genes. Odds ratios were estimated for non-Hispanic whites and several ethnic subgroups using 2-sided tests. Consistent with previous findings, odds ratios were increased for "new" participant TNF -308A carriers (NHL: per-allele odds ratio (ORallelic) = 1.10, P-trend = 0.001; diffuse large B-cell lymphoma (DLBCL): ORallelic = 1.23, P-trend = 0.004). In the combined population, odds ratios were increased for TNF -308A carriers (NHL: ORallelic = 1.13, P-trend = 0.0001; DLBCL: ORallelic = 1.25, P-trend = 3.7 x 10(-6); marginal zone lymphoma: ORallelic = 1.35, P-trend = 0.004) and LTA 252G carriers (DLBCL: ORallelic = 1.12, P-trend = 0.006; mycosis fungoides: ORallelic = 1.44, P-trend = 0.015). The LTA 252A 〉 G/TNF -308G 〉 A haplotype containing the LTA/TNF variant alleles was strongly associated with DLBCL (P = 2.9 x 10(-8)). Results suggested associations between IL10 -3575T 〉 A and DLBCL (P-trend = 0.02) and IL10 -1082A 〉 G and mantle cell lymphoma (P-trend = 0.04). These findings strengthen previous results for DLBCL and the LTA 252A 〉 G/TNF -308A locus and provide robust evidence that these TNF/LTA gene variants, or others in linkage disequilibrium, are involved in NHL etiology
    Type of Publication: Journal article published
    PubMed ID: 20047977
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  • 3
    Keywords: CELLS ; EXPRESSION ; carcinoma ; RISK ; GENE ; leukemia ; MYC ; GENOME-WIDE ASSOCIATION ; NEBULETTE ; 19P13
    Abstract: Genome-wide association studies (GWAS) have identified four susceptibility loci for epithelial ovarian cancer (EOC), with another two suggestive loci reaching near genome-wide significance. We pooled data from a GWAS conducted in North America with another GWAS from the UK. We selected the top 24,551 SNPs for inclusion on the iCOGS custom genotyping array. We performed follow-up genotyping in 18,174 individuals with EOC (cases) and 26,134 controls from 43 studies from the Ovarian Cancer Association Consortium. We validated the two loci at 3q25 and 17q21 that were previously found to have associations close to genome-wide significance and identified three loci newly associated with risk: two loci associated with all EOC subtypes at 8q21 (rs11782652, P = 5.5 x 10(-9)) and 10p12 (rs1243180, P = 1.8 x 10(-8)) and another locus specific to the serous subtype at 17q12 (rs757210, P = 8.1 x 10(-10)). An integrated molecular analysis of genes and regulatory regions at these loci provided evidence for functional mechanisms underlying susceptibility and implicated CHMP4C in the pathogenesis of ovarian cancer.
    Type of Publication: Journal article published
    PubMed ID: 23535730
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  • 4
    Keywords: GENE ; MOLECULAR CHARACTERIZATION ; SUSCEPTIBILITY LOCUS ; VARIANTS ; IDENTIFICATION ; microsatellite instability ; MUTATIONS ; endometriosis ; CLEAR-CELL CARCINOMA ; GRADE SEROUS CARCINOMA
    Abstract: Epithelial ovarian cancer (EOC) is a heterogeneous cancer with both genetic and environmental risk factors. Variants influencing the risk of developing the less-common EOC subtypes have not been fully investigated. We performed a genome-wide association study (GWAS) of EOC according to subtype by pooling genomic DNA from 545 cases and 398 controls of European descent, and testing for allelic associations. We evaluated for replication 188 variants from the GWAS [56 variants for mucinous, 55 for endometrioid and clear cell, 53 for low-malignant potential (LMP) serous, and 24 for invasive serous EOC], selected using pre-defined criteria. Genotypes from 13,188 cases and 23,164 controls of European descent were used to perform unconditional logistic regression under the log-additive genetic model; odds ratios (OR) and 95 % confidence intervals are reported. Nine variants tagging six loci were associated with subtype-specific EOC risk at P 〈 0.05, and had an OR that agreed in direction of effect with the GWAS results. Several of these variants are in or near genes with a biological rationale for conferring EOC risk, including ZFP36L1 and RAD51B for mucinous EOC (rs17106154, OR = 1.17, P = 0.029, n = 1,483 cases), GRB10 for endometrioid and clear cell EOC (rs2190503, P = 0.014, n = 2,903 cases), and C22orf26/BPIL2 for LMP serous EOC (rs9609538, OR = 0.86, P = 0.0043, n = 892 cases). In analyses that included the 75 GWAS samples, the association between rs9609538 (OR = 0.84, P = 0.0007) and LMP serous EOC risk remained statistically significant at P 〈 0.0012 adjusted for multiple testing. Replication in additional samples will be important to verify these results for the less-common EOC subtypes.
    Type of Publication: Journal article published
    PubMed ID: 24190013
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