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  • EXPRESSION  (9)
  • Analytical Chemistry and Spectroscopy  (7)
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  • 1
    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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  • 2
    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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  • 3
    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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  • 4
    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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  • 5
    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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  • 6
    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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  • 7
    Keywords: CANCER ; EXPRESSION ; SURVIVAL ; CLASSIFICATION ; DIAGNOSIS ; INFORMATION ; SYSTEM ; COHORT ; DISEASE ; RISK ; GENE ; GENE-EXPRESSION ; GENES ; microarray ; validation ; PATIENT ; prognosis ; SEQUENCE ; SEQUENCES ; IDENTIFICATION ; AMPLIFICATION ; gene expression ; MICROARRAY DATA ; microarrays ; DESIGN ; NUMBER ; CANCER-PATIENTS ; PREDICTION ; SELECTION ; CANCER PATIENTS ; neuroblastoma ; ONCOLOGY ; GENE-EXPRESSION PROFILES ; development ; prospective ; RISK STRATIFICATION ; outcome ; SIGNATURES ; EXPRESSION SIGNATURES ; STRATIFICATION
    Abstract: Purpose: Reliable prognostic stratification remains a challenge for cancer patients, especially for diseases with variable clinical course such as neuroblastoma. Although numerous studies have shown that outcome might be predicted using gene expression signatures, independent cross-platform validation is often lacking. Experimental Design: Using eight independent studies comprising 933 neuroblastoma patients, a prognostic gene expression classifier was developed, trained, tested, and validated. The classifier was established based on reanalysis of four published studies with updated clinical information, reannotation of the probe sequences, common risk definition for training cases, and a single method for gene selection (prediction analysis of microarray) and classification (correlation analysis). Results: Based on 250 training samples from four published microarray data sets, a correlation signature was built using 42 robust prognostic genes. The resulting classifier was validated on 351 patients from four independent and unpublished data sets and on 129 remaining test samples from the published studies. Patients with divergent outcome in the total cohort, as well as in the different risk groups, were accurately classified (log-rank P 〈 0.001 for overall and progression-free survival in the four independent data sets). Moreover, the 42-gene classifier was shown to be an independent predictor for survival (odds ratio, 〉5). Conclusion: The strength of this 42-gene classifier is its small number of genes and its cross-platform validity in which it outperforms other published prognostic signatures. The robustness and accuracy of the classifier enables prospective assessment of neuroblastoma patient outcome. Most importantly, this gene selection procedure might be an example for development and validation of robust gene expression signatures in other cancer entities. Clin Cancer Res; 16(5); 1532-41. (C)2010 AACR
    Type of Publication: Journal article published
    PubMed ID: 20179214
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  • 8
    Keywords: EXPRESSION ; SURVIVAL ; Germany ; MODEL ; MODELS ; CLASSIFICATION ; DIAGNOSIS ; COHORT ; DEATH ; DISEASE ; MORTALITY ; RISK ; GENE ; GENE-EXPRESSION ; microarray ; PATIENT ; MARKER ; IMPACT ; STAGE ; AMPLIFICATION ; gene expression ; microarrays ; AGE ; MARKERS ; HIGH-RISK ; STRATEGIES ; SPONTANEOUS REGRESSION ; PREDICTION ; INFANTS ; pathology ; CHILDREN ; MICROARRAY ANALYSIS ; neuroblastoma ; ONCOLOGY ; REGRESSION ; overall survival ; INDEPENDENT PROGNOSTIC MARKER ; methods ; PROGNOSTIC MARKER ; PROFILES ; EXPRESSION PROFILES ; RISK STRATIFICATION ; SUBGROUPS ; MYC ; PROFILE ; outcome ; STRATEGY ; CONTRIBUTE ; COHORTS ; COX REGRESSION ; clinical oncology ; STRATIFICATION ; prognostic
    Abstract: Purpose To evaluate the impact of a predefined gene expression - based classifier for clinical risk estimation and cytotoxic treatment decision making in neuroblastoma patients. Patients and Methods Gene expression profiles of 440 internationally collected neuroblastoma specimens were investigated by microarray analysis, 125 of which were examined prospectively. Patients were classified as either favorable or unfavorable by a 144- gene prediction analysis for microarrays (PAM) classifier established previously on a separate set of 77 patients. PAM classification results were compared with those of current prognostic markers and risk estimation strategies. Results The PAM classifier reliably distinguished patients with contrasting clinical courses (favorable [n = 249] and unfavorable [n = 191]; 5- year event free survival [EFS] 0.84 +/- 0.03 v 0.38 +/- 0.04; 5-year overall survival [OS] 0.98 +/- 0.01 v 0.56 +/- 0.05, respectively; both P = .001). Moreover, patients with divergent outcome were robustly discriminated in both German and international cohorts and in prospectively analyzed samples (P = .001 for both EFS and OS for each). In subgroups with clinical low-, intermediate-, and high-risk of death from disease, the PAM predictor significantly separated patients with divergent outcome (low-risk 5-year OS: 1.0 v 0.75 +/- 0.10, P = .001; intermediaterisk: 1.0 v 0.82 +/- 0.08, P = .042; and high-risk: 0.81 +/- 0.08 v 0.43 = 0.05, P=.001). In multivariate Cox regression models based on both EFS and OS, PAM was a significant independent prognostic marker (EFS: hazard ratio [HR], 3.375; 95% CI, 2.075 to 5.492; P=.001; OS: HR, 11.119, 95% CI, 2.487 to 49.701; P=.001). The highest potential clinical impact of the classifier was observed in patients currently considered as non - high- risk (n= 289; 5- year EFS: 0.87= 0.02 v 0.44= 0.07; 5- year OS: 1.0 v 0.80= 0.06; both P=.001). Conclusion Gene expression - based classification using the 144- gene PAM predictor can contribute to improved treatment stratification of neuroblastoma patients
    Type of Publication: Journal article published
    PubMed ID: 20567016
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  • 9
    Keywords: CANCER ; EXPRESSION ; tumor ; DISEASE ; RISK ; TUMORS ; DNA ; MARKER ; SEQUENCE ; ASSOCIATION ; SUSCEPTIBILITY ; VARIANTS ; MUTATION ; genetics ; BLADDER ; BLADDER-CANCER ; MARKERS ; RECURRENCE ; MUTATIONS ; NETHERLANDS ; VARIANT ; SOMATIC MUTATIONS ; UROTHELIAL CELL-CARCINOMA ; Genetic ; FGFR3 MUTATIONS
    Abstract: Previously, we reported germline DNA variants associated with risk of urinary bladder cancer (UBC) in Dutch and Icelandic subjects. Here we expanded the Icelandic sample set and tested the top 20 markers from the combined analysis in several European case-control sample sets, with a total of 4,739 cases and 45,549 controls. The T allele of rs798766 on 4p16.3 was found to associate with UBC (odds ratio = 1.24, P = 9.9 x 10(-12)). rs798766 is located in an intron of TACC3, 70 kb from FGFR3, which often harbors activating somatic mutations in low-grade, noninvasive UBC. Notably, rs798766[T] shows stronger association with low-grade and low-stage UBC than with more aggressive forms of the disease and is associated with higher risk of recurrence in low-grade stage Ta tumors. The frequency of rs798766[T] is higher in Ta tumors that carry an activating mutation in FGFR3 than in Ta tumors with wild-type FGFR3. Our results show a link between germline variants, somatic mutations of FGFR3 and risk of UBC.
    Type of Publication: Journal article published
    PubMed ID: 20348956
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  • 10
    ISSN: 0935-6304
    Keywords: Gas chromatography, GC ; Glass capillary columns ; Free release static coating ; Chemistry ; Analytical Chemistry and Spectroscopy
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Notes: The coating speed upon static coating of glass capillary columans was evaluated in terms of inner diameter and length of the column, viscosity and pressure of solvent vapor, etc. From the equation obtained it can be shown that a smaller diameter of a microbore column restricts solvent vapor transfer to the orifice of the column drastically. To compensate for this restriction, a higher pressure at the meniscus is needed. As an alternative to using a higher coating temperature, application of more volatile solvents such as n-butane and isobutane is proposed. Several glass capillary columns (130 μm i.d.) were coated with SE-54 dissolved inpentane-acetone mixed with n-butane or isobutane and the column performances were evaluated. Selection of these solvents permitted free release static coating of ca. 100 μm columns at lower or even ambient temperatures and they were equally suitable as commonly applied solvents (e.g. pentane) to coat highly efficient columns.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
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