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  • 1
    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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  • 2
    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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  • 3
    Keywords: SPECTRA ; SURVIVAL ; Germany ; CLASSIFICATION ; GENE ; GENE-EXPRESSION ; HYBRIDIZATION ; RNA ; COMPLEX ; COMPLEXES ; IN-SITU ; COMPARATIVE GENOMIC HYBRIDIZATION ; cytogenetics ; LYMPHOMA ; gene expression ; chemotherapy ; FUSION ; leukemia ; C-MYC ; gene expression profiling ; ORGANIZATION ; B-CELL LYMPHOMA ; NON-HODGKINS-LYMPHOMA ; in situ hybridization ; TRANSLOCATIONS ; LOCUS ; LYMPHOMAS ; molecular signature ; SUBGROUPS
    Abstract: Background: The distinction between Burkitt's lymphoma and diffuse large-B-cell lymphoma is unclear. We used transcriptional and genomic profiling to define Burkitt's lymphoma more precisely and to distinguish subgroups in other types of mature aggressive B-cell lymphomas. Methods: We performed gene-expression profiling using Affymetrix U133A GeneChips with RNA from 220 mature aggressive B-cell lymphomas, including a core group of 8 Burkitt's lymphomas that met all World Health Organization (WHO) criteria. A molecular signature for Burkitt's lymphoma was generated, and chromosomal abnormalities were detected with interphase fluorescence in situ hybridization and array-based comparative genomic hybridization. Results: We used the molecular signature for Burkitt's lymphoma to identify 44 cases: 11 had the morphologic features of diffuse large-B-cell lymphomas, 4 were unclassifiable mature aggressive B-cell lymphomas, and 29 had a classic or atypical Burkitt's morphologic appearance. Also, five did not have a detectable IG-myc Burkitt's translocation, whereas the others contained an IG-myc fusion, mostly in simple karyotypes. Of the 176 lymphomas without the molecular signature for Burkitt's lymphoma, 155 were diffuse large-B-cell lymphomas. Of these 155 cases, 21 percent had a chromosomal breakpoint at the myc locus associated with complex chromosomal changes and an unfavorable clinical course. Conclusions: Our molecular definition of Burkitt's lymphoma clarifies and extends the spectrum of the WHO criteria for Burkitt's lymphoma. In mature aggressive B-cell lymphomas without a gene signature for Burkitt's lymphoma, chromosomal breakpoints at the myc locus were associated with an adverse clinical outcome
    Type of Publication: Journal article published
    PubMed ID: 16760442
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  • 4
    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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  • 5
    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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  • 6
    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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