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  • ASSOCIATION  (12)
  • EXPRESSION  (9)
  • 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 ; 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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  • 4
    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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  • 5
    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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  • 6
    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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  • 7
    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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  • 8
    Keywords: EXPRESSION ; carcinoma ; RISK ; ORAL-CONTRACEPTIVES ; GROWTH-FACTOR-BETA ; TRENDS ; MAMMARY-GLAND ; TGF-BETA ; DECORIN ; GENOME-WIDE ASSOCIATION
    Abstract: Alterations in stromal tissue components can inhibit or promote epithelial tumorigenesis. Decorin (DCN) and lumican (LUM) show reduced stromal expression in serous epithelial ovarian cancer (sEOC). We hypothesized that common variants in these genes associate with risk. Associations with sEOC among Caucasians were estimated with odds ratios (OR) among 397 cases and 920 controls in two U. S.-based studies (discovery set), 436 cases and 1,098 controls in Australia (replication set 1) and a consortium of 15 studies comprising 1,668 cases and 4,249 controls (replication set 2). The discovery set and replication set 1 (833 cases and 2,013 controls) showed statistically homogeneous (P-heterogeneity 〉= 0.48) decreased risks of sEOC at four variants: DCN rs3138165, rs13312816 and rs516115, and LUM rs17018765 (OR = 0.6 to 0.9; P-trend = 0.001 to 0.03). Results from replication set 2 were statistically homogeneous (P-heterogeneity 〉= 0.13) and associated with increased risks at DCN rs3138165 and rs13312816, and LUM rs17018765: all ORs = 1.2; P-trend 〈= 0.02. The ORs at the four variants were statistically heterogeneous across all 18 studies (P-heterogeneity 〈= 0.03), which precluded combining. In post-hoc analyses, interactions were observed between each variant and recruitment period (P-interaction 〈= 0.003), age at diagnosis (P-interaction=0.04), and year of diagnosis (P-interaction=0.05) in the five studies with available information (1,044 cases, 2,469 controls). We conclude that variants in DCN and LUM are not directly associated with sEOC, and that confirmation of possible effect modification of the variants by non-genetic factors is required
    Type of Publication: Journal article published
    PubMed ID: 21637745
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  • 9
    Keywords: PEPTIDE ; EXPRESSION ; TOOL ; RISK ; VARIANTS ; CLASS-I ; SNPs ; RESOURCE ; SET ; UNIVERSITY
    Abstract: Genome-wide association studies (GWASs) of follicular lymphoma (FL) have previously identified human leukocyte antigen (HLA) gene variants. To identify additional FL susceptibility loci, we conducted a large-scale two-stage GWAS in 4,523 case subjects and 13,344 control subjects of European ancestry. Five non-HLA loci were associated with FL risk: 11q23.3 (rs4938573, p = 5.79 x 10(-20)) near CXCR5; 11q24.3 (rs4937362, p = 6.76 x 10(-11)) near ETS1; 3q28 (rs6444305, p = 1.10 x 10(-10)) in LPP; 18q21.33 (rs17749561, p = 8.28 x 10(-10)) near BCL2; and 8q24.21 (rs13254990, p = 1.06 x 10(-8)) near PVT1. In an analysis of the HLA region, we identified four linked HLA-DRbeta1 multiallelic amino acids at positions 11, 13, 28, and 30 that were associated with FL risk (pomnibus = 4.20 x 10(-67) to 2.67 x 10(-70)). Additional independent signals included rs17203612 in HLA class II (odds ratio [ORper-allele] = 1.44; p = 4.59 x 10(-16)) and rs3130437 in HLA class I (ORper-allele = 1.23; p = 8.23 x 10(-9)). Our findings further expand the number of loci associated with FL and provide evidence that multiple common variants outside the HLA region make a significant contribution to FL risk.
    Type of Publication: Journal article published
    PubMed ID: 25279986
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  • 10
    Keywords: EXPRESSION ; DISEASES ; RISK ; POLYMORPHISMS ; DNA-REPAIR GENES ; METAANALYSIS ; UROTHELIAL CELL-CARCINOMA ; imputation ; CONFERS SUSCEPTIBILITY ; SEQUENCE VARIANT
    Abstract: Genome-wide association studies (GWAS) of urinary bladder cancer (UBC) have yielded common variants at 12 loci that associate with risk of the disease. We report here the results of a GWAS of UBC including 1670 UBC cases and 90 180 controls, followed by replication analysis in additional 5266 UBC cases and 10 456 controls. We tested a dataset containing 34.2 million variants, generated by imputation based on whole-genome sequencing of 2230 Icelanders. Several correlated variants at 20p12, represented by rs62185668, show genome-wide significant association with UBC after combining discovery and replication results (OR = 1.19, P = 1.5 x 10(-11) for rs62185668-A, minor allele frequency = 23.6%). The variants are located in a non-coding region approximately 300 kb upstream from the JAG1 gene, an important component of the Notch signaling pathways that may be oncogenic or tumor suppressive in several forms of cancer. Our results add to the growing number of UBC risk variants discovered through GWAS.
    Type of Publication: Journal article published
    PubMed ID: 24861552
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