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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: 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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  • 3
    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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  • 4
    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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  • 5
    Keywords: GENOME ; IDENTIFICATION ; MUTATION ; ABERRATIONS ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; MULTIPLE-MYELOMA ; BREAKPOINTS ; HODGKIN-LYMPHOMA ; GENE TRANSLOCATIONS ; DEREGULATION
    Abstract: Translocations affecting chromosome subband 6p25.3 containing the IRF4 gene have been recently described as characteristic alterations in a molecularly distinct subset of germinal center B-cell-derived lymphomas. Secondary changes have yet only been described in few of these lymphomas. Here, we performed array-comparative genomic hybridization and molecular inversion probe microarray analyses on DNA from 12 formalin-fixed paraffin-embedded and two fresh-frozen IRF4 translocation-positive lymphomas, which together with the previously published data on nine cases allowed the extension of copy number analyses to a total of 23 of these lymphomas. All except one case carried chromosomal imbalances, most frequently gains in Xq28, 11q22.3-qter, and 7q32.1-qter and losses in 6q13-16.1, 15q14-22.31, and 17p. No recurrent copy-neutral losses of heterozygosity were observed. TP53 point mutations were detected in three of six cases with loss of 17p. Overall this study unravels a recurrent pattern of secondary genetic alterations in IRF4 translocation-positive lymphomas. (c) 2012 Wiley Periodicals, Inc.
    Type of Publication: Journal article published
    PubMed ID: 23073988
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