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  • 1
    Keywords: CANCER ; EXPRESSION ; tumor ; carcinoma ; CELL ; Germany ; incidence ; GENE ; GENES ; HYBRIDIZATION ; microarray ; cell line ; DIFFERENTIATION ; TISSUE ; LINES ; ACTIVATION ; DNA ; FAMILY ; CELL-LINES ; MEMBER ; MEMBERS ; BREAST-CANCER ; cytokines ; IDENTIFICATION ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; microarrays ; NUMBER ; CHROMOSOMAL-ABERRATIONS ; CELL-LINE ; LINE ; PCR ; REGION ; REGIONS ; adenocarcinoma ; CANCER-RESEARCH ; FREQUENT ; REVEALS ; IMBALANCES ; OVEREXPRESSION ; cell lines ; pancreatic cancer ; pancreatic carcinoma ; GENOMIC HYBRIDIZATION ; HIGH-LEVEL ; CYTOKINE ; ONCOLOGY ; SUBSET ; RE ; PANCREATIC-CANCER ; FAMILIES ; AMPLIFICATIONS ; LEADS ; CANDIDATE GENES ; REAL-TIME ; EGFR ; MALT-LYMPHOMA
    Abstract: Genomic analyses aimed at the detection of high-level DNA amplifications were performed on 13 widely used pancreatic cancer cell lines and 6 pancreatic tumor specimens. For these analyses, array-based comparative genomic hybridization (Matrix-CGH) onto dedicated microarrays was used. In comparison with chromosomal CGH (eight amplifications), a 〉3-fold number of DNA amplifications was detected (n = 29). The most frequent amplifications mapped to 7p12.3 (three pancreatic cancer cell lines and three pancreatic tumor specimens), 8q24 (four pancreatic cancer cell lines and one pancreatic tumor specimen), 11q13 (three pancreatic cancer cell lines and three pancreatic tumor specimens), and 20q13 (four pancreatic cancer cell lines and three pancreatic tumor specimens). Genes contained in the consensus regions were MYC (8q24), EGFR (7p12.3), and FGF3 (11q13). In six of seven pancreatic cancer cell lines and pancreatic tumor specimens with 20q13 amplifications, the novel candidate gene NFAT C2, which plays a role in the activation of cytokines, was amplified. Other amplifications also affected genes for which a pathogenetic role in pancreatic carcinoma has not been described, such as BCL10 and BCL6, two members of the BCL family. A subset of amplified genes was checked for overexpression by means of real-time PCR, revealing the highest expression levels for BCL6 and BCL10. Thus, Matrix-CGH allows the detection of a high number of amplifications, resulting in the identification of novel candidate genes in pancreatic cancer
    Type of Publication: Journal article published
    PubMed ID: 15231651
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  • 2
    Keywords: APOPTOSIS ; EXPRESSION ; tumor ; CELL ; Germany ; human ; GENE ; GENES ; HYBRIDIZATION ; microarray ; PROTEIN ; SAMPLE ; SAMPLES ; transcription ; cell line ; RESOLUTION ; LINES ; NF-KAPPA-B ; ACTIVATION ; DNA ; primary ; BASE ; ANTIGEN ; CELL-LINES ; FREQUENCY ; FREQUENCIES ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; COPY NUMBER ; immunohistochemistry ; LYMPHOMA ; NUMBER ; CELL-LINE ; leukemia ; LINE ; REGION ; REGIONS ; LOCALIZATION ; leukocyte ; NF-kappa B ; DNA AMPLIFICATION ; CHROMOSOMAL LOCALIZATION ; cell lines ; GAINS ; non-hodgkin's lymphoma ; B-CELL LYMPHOMA ; HIGH-FREQUENCY ; MATRIX ; FEATURES ; ONCOLOGY ; HIGH-RESOLUTION ; CANDIDATE GENES ; DEFECTS ; ACTIVATOR ; analysis ; GENOTYPE ; LOSSES ; CANDIDATE ; HODGKIN LYMPHOMA ; genomic ; DEFECT ; B-CELL ; GENOMIC ALTERATIONS ; ARRAY CGH ; ARRAY-CGH ; POINT ; DNA-CHIP HYBRIDIZATION ; mediastinal B-cell lymphoma ; array-based comparative genomic hybridization ; NUCLEAR ACCUMULATION
    Abstract: Primary mediastinal B-cell lymphoma (PMBL) is an aggressive extranodal B-cell non-Hodgkin's lymphoma with specific clinical, histopathological and genomic features. To characterize further the genotype of PMBL, we analyzed 37 tumor samples and PMBL cell lines Med-B1 and Karpas1106P using array-based comparative genomic hybridization (matrix- or array-CGH) to a 2.8k genomic microarray. Due to a higher genomic resolution, we identified altered chromosomal regions in much higher frequencies compared with standard CGH: for example, +9p24 (68%), +2p15 (51%), +7q22 (32%), +9q34 (32%), +11q23 (18%), +12q (30%) and +18q21 (24%). Moreover, previously unknown small interstitial chromosomal low copy number alterations (for example, -6p21, -11q13.3) and a total of 19 DNA amplifications were identified by array-CGH. For 17 chromosomal localizations (10 gains and 7 losses), which were altered in more than 10% of the analyzed cases, we delineated minimal consensus regions based on genomic base pair positions. These regions and selected immunohistochemistries point to candidate genes that are discussed in the context of NF-kappa B transcription activation, human leukocyte antigen class I/II defects, impaired apoptosis and Janus kinase/signal transducer and activator of transcription (JAK/STAT) activation. Our data confirm the genomic uniqueness of this tumor and provide physically mapped genomic regions of interest for focused candidate gene analysis
    Type of Publication: Journal article published
    PubMed ID: 17728785
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  • 3
    Keywords: EXPRESSION ; SURVIVAL ; CELL ; CLINICAL-TRIAL ; Germany ; THERAPY ; TOOL ; DISTINCT ; GENOME ; HYBRIDIZATION ; microarray ; validation ; DNA ; treatment ; chromosome ; DISCOVERY ; CLINICAL-TRIALS ; chemotherapy ; leukemia ; ABERRATIONS ; MARKERS ; FRAGMENTS ; IMBALANCES ; CD38 EXPRESSION ; MANTLE CELL LYMPHOMA ; NON-HODGKINS-LYMPHOMA ; AMPLIFICATIONS ; DNA COPY NUMBER ; GENE MUTATION STATUS
    Abstract: B cell chronic lymphocytic leukemia (B-CLL) is characterized by a highly variable clinical course. Recurrent chromosomal imbalances provide significant prognostic markers. Risk-adapted therapy based on genomic alterations-has become an option that is currently being tested in clinical trials. To supply a robust tool for such large scale studies, we developed a comprehensive DNA microarray dedicated to the automated analysis of recurrent genomic imbalances in B-CLL by array-based comparative genomic hybridization (matrix-CGH). Validation of this chip in a series of 106 B-CLL cases revealed a high specificity and sensitivity that fulfils the criteria for application in clinical oncology. This chip is immediately applicable within clinical B-CLL treatment trials that evaluate whether B-CLL cases with distinct chromosomal abnormalities should be treated with chemotherapy of different intensities and/or stem cell transplantation. Through the control set of DNA fragments equally distributed over the genome, recurrent genomic imbalances were discovered: trisomy of chromosome 19 and gain of the MYCN oncogene correlating With an elevation of MYCN mRNA expression
    Type of Publication: Journal article published
    PubMed ID: 14730057
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  • 4
    Keywords: EXPRESSION ; SURVIVAL ; tumor ; Germany ; neoplasms ; GENE ; GENES ; GENOME ; HYBRIDIZATION ; microarray ; SAMPLE ; SAMPLES ; transcription ; ACTIVATION ; DNA ; mechanisms ; TARGET ; STAGE ; IN-SITU ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; LYMPHOMA ; DNA microarray ; microarrays ; ABERRATIONS ; DELETIONS ; POLYMERASE-CHAIN-REACTION ; DNA AMPLIFICATION ; FLUORESCENCE ; gene amplification ; IMBALANCES ; GAINS ; B-CELL LYMPHOMA ; CGH ; matrix-CGH ; DNA COPY-NUMBER
    Abstract: DNA amplifications are important mechanisms for protooncogene activation. Comparative genomic hybridization (CGH) to metaphase chromosome preparations has revealed amplifications in 10-20% of B-cell lymphomas (B-NHL). We analysed a series of 16 aggressive non-Hodgkin lymphomas by the new approach termed Matrix-CGH (M-CGH) using genomic DNA microarrays as hybridization target. For M-CGH, a dedicated B-cell lymphoma chip was constructed containing 496 genomic targets covering oncogenes, tumor suppressor genes as well as chromosome regions frequently altered in B-NHL. In 10 of 16 samples a total of 15 DNA amplifications were identified. The amplicons included BCL2, REL, CCND1, CCND2, JAK2, FGF4 and MDM2. Four of the 15 amplifications remained undetected by chromosomal CGH. The respective amplicons mapped to bands 2p13, 9p13-p21 and 12q24 and, were confirmed by fluorescence in situ hybridization. Furthermore, for four genomically amplified genes real-time quantitative reverse transcription polymerase chain reaction revealed elevated mRNA expression levels. These data show the superior diagnostic sensitivity of the newly developed diagnostic tool. As only a small portion of the genome (approximately 1.5%) has been analysed by the present DNA array, it is likely that gene amplifications are much more common in aggressive lymphomas than previously assumed
    Type of Publication: Journal article published
    PubMed ID: 12618769
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  • 5
    Keywords: CANCER ; tumor ; Germany ; SITE ; SITES ; GENE ; GENES ; HYBRIDIZATION ; TISSUE ; TUMORS ; RESOLUTION ; PATIENT ; DNA ; CELL-LINES ; SEQUENCE ; SEQUENCES ; chromosome ; BREAST ; breast cancer ; BREAST-CANCER ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; OVARIAN-CANCER ; IN-SITU HYBRIDIZATION ; PCR ; DATABASE ; REGION ; PROGNOSTIC-SIGNIFICANCE ; IMBALANCES ; C-MYC ; GAINS ; CHROMOSOMAL IMBALANCES ; 1p ; TUMOR-SUPPRESSOR ; CANDIDATE GENES ; SOLID TUMORS ; DNA COPY NUMBER ; PROTOONCOGENE ; CHIP ; SUPPRESSOR ; tumor suppressor gene ; SUPPRESSOR GENES ; 9P ; HIGH-RESOLUTION ANALYSIS ; UNDERGO AMPLIFICATION
    Abstract: Genomic imbalances in 31 formalin-fixed and paraffin-embedded primary tumors of advanced breast cancer were analyzed by microarray-based comparative genomic hybridization (matrix-CGH). A DNA chip was designed comprising 422 mapped genomic sequences including 47 proto-oncogenes, 15 tumor suppressor genes, as well as frequently imbalanced chromosomal regions. Analysis of the data was challenging due to the impaired quality of DNA prepared from paraffin-embedded samples. Nevertheless, using a method for the statistical evaluation of the balanced state for each individual experiment, we were able to reveal imbalances with high significance, which were in good concordance with previous data collected by chromosomal CGH from the same patients. Owing to the improved resolution of matrix-CGH, genomic imbalances could be narrowed down to the level of individual bacterial artificial chromosome and P1-derived artificial chromosome clones. On average 37 gains and 13 losses per tumor cell genome were scored. Gains in more than 30% of the cases were found on 1p, 1q, 6p, 7p, 8q, 9q, 11q, 12q, 17p, 17q, 20q, and 22q, and losses on 6q, 9p, 11q, and 17p. Of the 51 chromosomal regions found amplified by matrix-CGH, only 12 had been identified by chromosomal CGH. Within these 51 amplicons, genome database information defined 112 candidate genes, 44 of which were validated by either PCR amplification of sequence tag sites or DNA sequence analysis
    Type of Publication: Journal article published
    PubMed ID: 15695385
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  • 6
    Keywords: SPECTRA ; EXPRESSION ; Germany ; screening ; GENE ; GENE-EXPRESSION ; GENES ; HYBRIDIZATION ; microarray ; MOLECULAR CHARACTERIZATION ; PATIENT ; COMPLEX ; COMPLEXES ; DNA ; IDENTIFICATION ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; gene expression ; microarrays ; leukemia ; PATHOGENESIS ; REGION ; REGIONS ; FRAGMENTS ; SEGMENTS ; IMBALANCES ; HEMATOPOIETIC-CELLS ; gene expression profiling ; expression profiling ; HIGH-LEVEL ; ACUTE MYELOGENOUS LEUKEMIA ; DNA COPY-NUMBER ; SUBSET ; CANDIDATE GENES ; ADULT PATIENTS ; LEVEL ; PROFILES ; LOSSES ; CANDIDATE ; genomic ; FRAGMENT ; COMMONLY DELETED REGION ; ARRAY CGH ; 8Q24 ; ARRAY-CGH ; DOUBLE MINUTE CHROMOSOMES ; MYELODYSPLASTIC SYNDROMES
    Abstract: Purpose To identify novel genomic regions of interest in acute myeloid leukemia (AML) with complex karyotypes, we applied comparative genomic hybridization to microarrays (array-CGH), allowing high-resolution genome-wide screening of genomic imbalances. Patients and Methods Sixty AML cases with complex karyotypes were analyzed using array-CGH; parallel analysis of gene expression was performed in a subset of cases. Results Genomic losses were found more frequently than gains. The most frequent losses affected 5q (77%), 17p (55%), and 7q (45%), and the most frequent genomic gains 11q (40%) and 8q (38%). Critical segments could be delineated to genomic fragments of only 0.8 to a few megabase-pairs of DNA. In lost/gained regions, gene expression profiling detected a gene dosage effect with significant lower/higher average gene expression levels across the genes located in the respective regions. Furthermore, high-level DNA amplifications were identified in several regions: 11q23.3-q24.1 (n=7), 21q22 (n=6), 11q23.3 (n=5), 13q12 (n=3), 8q24 (n=3), 9p24 (n=2), 12p13 (n=2), and 20q11 (n=2). Parallel analysis of gene expression in critical amplicons displayed overexpressed candidate genes (eg, C8FW and MYC in 8q24). Conclusion In conclusion, a large spectrum of genomic imbalances, including novel recurring, changes in AML with complex karyotypes, was identified using array-CGH. In addition, the combined analysis of array-CGH data with gene expression profiles allowed the detection of candidate genes involved in the pathogenesis of AML
    Type of Publication: Journal article published
    PubMed ID: 16864856
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  • 7
    Keywords: EXPRESSION ; tumor ; GENE ; HYBRIDIZATION ; microarray ; DNA ; IDENTIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; COPY-NUMBER ; LYMPHOMA ; DNA microarray ; ACUTE LYMPHOBLASTIC-LEUKEMIA ; FRAGMENTS ; PREDICTIVE MODEL ; CDNA MICROARRAYS ; non-hodgkin's lymphoma ; B-CELL LYMPHOMA ; FOLLICULAR LYMPHOMA ; CHRONIC LYMPHOCYTIC- LEUKEMIA ; expression and genomic profiling ; GENE-EXPRESSION PROFILE ; matrix-CGH ; NON-HODGKINS-LYMPHOMA
    Abstract: Recently, DNA microarray technology has opened new avenues for the understanding of lymphomas. By hybridization of cDNA to arrays containing 〉10,000 different DNA fragments, this approach allows the simultaneous evaluation of the mRNA expression of thousands of genes in a single experiment. Using sophisticated bioinformatic tools, the huge amount of raw data can be clustered resulting in (1) tumor subclassification, (2) identification of pathogenetically relevant genes, or (3) biological predictors for the clinical course. This approach already has provided novel insights into different entities of B-cell non-Hodgkin's lymphomas. Genomic DNA chip hybridization (matrix-CGH) is a complementary approach focussing on genomic aberrations. In this review, we discuss the impact of this new technology both with regard to methodological aspects as well as to novel findings influencing our understanding of lymphomas
    Type of Publication: Journal article published
    PubMed ID: 12719886
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  • 8
    Keywords: CANCER ; SURVIVAL ; tumor ; CELL ; Germany ; human ; GENE ; GENES ; HYBRIDIZATION ; SAMPLE ; SAMPLES ; MOLECULAR CHARACTERIZATION ; PATIENT ; DNA ; PAIRS ; chromosome ; FREQUENCY ; DELETION ; IDENTIFICATION ; IN-SITU ; COMPARATIVE GENOMIC HYBRIDIZATION ; LYMPHOMA ; NUMBER ; leukemia ; ABERRATIONS ; DELETIONS ; TUMOR-SUPPRESSOR GENE ; REGION ; PROGNOSTIC-FACTORS ; REGIONS ; ONCOGENE ; FLUORESCENCE ; ATM GENE ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; MANTLE CELL LYMPHOMA ; HIGH-FREQUENCY ; NON-HODGKINS-LYMPHOMA ; F ; ONCOLOGY ; CHROMOSOME-TRANSLOCATION ; H MUTATION STATUS
    Abstract: Tumor samples of 53 patients with t(11;14)-positive mantle cell lymphomas (MCLs) were analyzed by matrix-based comparative genomic hybridization (matrix-CGH) using a dedicated DNA array. In 49 cases, genomic aberrations were identified. In comparison to chromosomal CGH, a 50%. higher number of aberrations was found and the high specificity of,matrix-CGH was demonstrated by fluorescence in situ hybridization (FISH) analyses. The 11q gains and 13q34 deletions, which have not been described as frequent genomic aberrations in MCL, were identified by matrix-CGH in 15 and 26 cases, respectively. For several genomic aberrations, novel consensus regions were defined: 8p21 (size of the consensus region, 2.4 megabase pairs [Mbp]; candidate genes: TNFRSF10B, TNFRSF10C, TNFRSF10D); 10p13 (2.7 Mbp; BM/1); 11q13 (1.4 Mbp; RELA); 11q13 (5.2 Mbp; CCND1); 13q14 (0.4 Mbp; RFP2, BCMSUN) and 13q34 (6.9 Mbp). In univariate analyses correlating genomic aberrations and clinical course, 8p- and 13q14- deletions were associated with an inferior overall survival. These data provide a basis for further studies focusing on the identification of pathogenetically or clinically relevant genes, in MCL
    Type of Publication: Journal article published
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  • 9
    Keywords: CELLS ; EXPRESSION ; CELL ; Germany ; human ; GENE ; GENES ; DIFFERENTIATION ; DNA ; TISSUES ; LYMPHOMA ; PATTERNS ; DNA methylation ; TARGETS ; INSIGHTS ; METHYLATION ; B-CELL LYMPHOMA ; DE-NOVO METHYLATION ; EMBRYONIC STEM-CELLS ; HUMAN CANCER ; development ; non-Hodgkin lymphoma ; BURKITTS-LYMPHOMA ; HEMATOPOIETIC TISSUES ; DEFINED FACTORS ; DEVELOPMENTAL REGULATORS ; INSTRUCTIVE MECHANISM
    Abstract: Lymphomas are assumed to originate at different stages of lymphocyte development through chromosomal aberrations. Thus, different lymphomas resemble lymphocytes at distinct differentiation stages and show characteristic morphologic, genetic, and transcriptional features. Here, we have performed a microarray-based DNA methylation profiling of 83 mature aggressive B-cell non-Hodgkin lymphomas (maB-NHLs) characterized for their morphologic, genetic, and transcriptional features, including molecular Burkitt lymphomas and diffuse large B-cell lymphomas. Hierarchic clustering indicated that methylation patterns in maB-NHLs were not strictly associated with morphologic, genetic, or transcriptional features. By supervised analyses, we identified 56 genes de novo methylated in all lymphoma subtypes studied and 22 methylated in a lymphoma subtype-specific manner. Remarkably, the group of genes de novo methylated in all lymphoma subtypes was significantly enriched for polycomb targets in embryonic stem cells. De novo methylated genes in all maB-NHLs studied were expressed at low levels in lymphomas and normal hematopoietic tissues but not in nonhematopoietic tissues. These findings, especially the enrichment for polycomb targets in stem cells, indicate that maB-NHLs with different morphologic, genetic, and transcriptional background share a similar stem cell-like epigenetic pattern. This suggests that maB-NHLs originate from cells with stem cell features or that stemness was acquired during lymphomagenesis by epigenetic remodeling. (Blood. 2009;113:2488-2497)
    Type of Publication: Journal article published
    PubMed ID: 19075189
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