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  • AMPLIFICATION  (5)
  • CANDIDATE GENES  (4)
  • 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 ; 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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  • 4
    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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  • 5
    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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