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  • 1
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    Keywords: RECEPTOR ; EXPRESSION ; Germany ; KINASE ; TYROSINE KINASE ; GENE ; GENE-EXPRESSION ; GENES ; transcription ; ACCURACY ; TRANSDUCTION ; PATIENT ; ACTIVATION ; DOMAIN ; cell cycle ; CELL-CYCLE ; CYCLE ; signal transduction ; IDENTIFICATION ; PATTERNS ; gene expression ; MUTATION ; SIGNAL-TRANSDUCTION ; leukemia ; REGION ; MUTATIONS ; PROGNOSTIC-SIGNIFICANCE ; CONSTITUTIVE ACTIVATION ; SERIES ; point mutation ; gene expression profiling ; CYCLE CONTROL ; HEMATOLOGIC MALIGNANCIES ; GENE-MUTATIONS ; ACUTE MYELOGENOUS LEUKEMIA ; acute myeloid leukemia ; NORMAL CYTOGENETICS ; STUDY-GROUP ULM ; CANDIDATE GENES ; INTERNAL TANDEM DUPLICATION ; MYELOID-LEUKEMIA ; GENE-TRANSCRIPTION ; ADULT PATIENTS ; HIGH-DOSE CYTARABINE ; EXPRESSION PATTERNS ; SIGNATURE ; COOPERATIVE-GROUP ; FLT3-activating mutations ; normal karyotype ; NRAS-activating mutations ; SONIC-HEDGEHOG
    Abstract: In acute myeloid leukemia (AML), constitutive activation of the FLT3 receptor tyrosine kinase, either by internal tandem duplications (FLT3-ITD) of the juxtamembrane region or by point mutations in the second tyrosine kinase domain (FLT3-TKD), as well as point mutations of the NRAS gene (NRAS-PM) are among the most frequent somatic gene mutations. To elucidate whether these mutations cause aberrant signal transduction in AML, we used gene expression pro. ling in a series of 110 newly diagnosed AML patients with normal karyotype. The different algorithms used for data analysis revealed highly concordant sets of genes, indicating that the identified gene signatures are specific for each analysed subgroup. Whereas samples with FLT3-ITD and FLT3-TKD could be separated with up to 100% accuracy, this did not apply for NRAS-PM and wild-type samples, suggesting that only FLT3-ITD and FLT3-TKD are associated with an apparent signature in AML. The set of discriminating genes included several known genes, which are involved in cell cycle control (CDC14A, WEE1), gene transcription (HOXB5, FOXA1), and signal transduction (SMG1). In conclusion, we showed that unique gene expression patterns can be correlated with FLT3-ITD and FLT3-TKD. This might lead to the identification of further pathogenetic relevant candidate genes particularly in AML with normal karyotype
    Type of Publication: Journal article published
    PubMed ID: 15674343
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  • 3
    Keywords: Germany ; ALGORITHM ; INFORMATION ; SYSTEM ; TOOL ; VISUALIZATION ; GENE-EXPRESSION ; PATTERNS ; DESIGN ; NUMBER ; Jun ; PROJECT ; INTEGRATION ; PROGRAM ; FRAMEWORK ; SOFTWARE ; TASK ; ANNOTATION ; GENOME DATABASE ; RESOURCE ; NEED ; DNA-MICROARRAY
    Abstract: Background: Interpreting the results of high-throughput experiments, such as those obtained from DNA-microarrays, is an often time-consuming task due to the high number of data-points that need to be analyzed in parallel. It is usually a matter of extensive testing and unknown beforehand, which of the possible approaches for the functional analysis will be the most informative Results: To address this problem, we have developed the Flexible Annotation and Correlation Tool (FACT). FACT allows for detection of important patterns in large data sets by simplifying the integration of heterogeneous data sources and the subsequent application of different algorithms for statistical evaluation or visualization of the annotated data. The system is constantly extended to include additional annotation data and comparison methods. Conclusion: FACT serves as a highly flexible framework for the explorative analysis of large genomic and proteomic result sets. The program can be used online; open source code and supplementary information are available at http://www.factweb.de
    Type of Publication: Journal article published
    PubMed ID: 15985174
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  • 4
    Keywords: Germany ; NETWORK ; SYSTEM ; SYSTEMS ; microarray ; FLOW ; DNA microarray ; DATABASE ; bioinformatics
    Abstract: QuickLIMS is a Microsoft Access-based laboratory information and management system, capable of processing all information for microarray production. The program's operational flow is protocol-based, dynamically adapting to changes of the process. It interacts with the laboratory robot and with other database systems over the network, and it represents a complete solution for the management of the entire manufacturing process. Availability and supplementary information: http://www.dkfz- heidelberg.de/kompl_genome/Other/QuickLims/index.html Contact: f.kokocinski@dkfz.de
    Type of Publication: Journal article published
    PubMed ID: 12538251
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  • 5
    Keywords: EXPRESSION ; GROWTH ; GROWTH-FACTOR ; proliferation ; tumor ; Germany ; PATHWAY ; PATHWAYS ; CLASSIFICATION ; GENE ; GENE-EXPRESSION ; GENES ; HYBRIDIZATION ; microarray ; PROTEIN ; meningioma ; TUMORS ; MESSENGER-RNA ; MARKER ; cell cycle ; CELL-CYCLE ; CYCLE ; chromosome ; PROGRESSION ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; MALIGNANCIES ; PATTERNS ; gene expression ; TUMOR PROGRESSION ; ABERRATIONS ; PATHOGENESIS ; BENIGN ; SELECTION ; gene expression profiling ; ORGANIZATION ; CDNA MICROARRAYS ; expression profiling ; CDNA MICROARRAY ; CHROMOSOMES ; MALIGNANCY ; PANCREATIC-CANCER ; TUMORIGENESIS ; CANDIDATE GENES ; GENOMIC ABERRATIONS ; regulation ; SUPPRESSOR ; PROFILES ; EXPRESSION PATTERNS ; IGFBP3 ; insulin-like growth factor ; EXPRESSION PROFILES ; MENINGIOMAS ; anaplastic ; HUMAN BRAIN-TUMORS ; IGF pathway ; WNT pathway
    Abstract: To identify gene expression profiles associated with human meningiomas of different World Health Organization (WHO) malignancy grades, we analyzed 30 tumors (13 benign meningiomas, WHO grade I; 12 atypical meningiomas, WHO grade II; 5 anaplastic meningiomas, WHO grade III) for the expression of 2,600 genes using cDNA-microarray technology. Receiver operator curve (ROC) analysis with a cutoff value of 45% selection probability identified 37 genes with decreased and 27 genes with increased expression in atypical and anaplastic meningiomas, compared to benign meningiomas. Supervised classification of the tumors did not reveal specific expression patterns representative of each WHO grade. However, anaplastic meningiomas could be distinguished from benign meningiomas by differential expression of a distinct set of genes, including several ones associated with cell cycle regulation and proliferation. Investigation of potential correlations between microarray expression data and genomic aberrations, detected by comparative genomic hybridization (CGH), demonstrated that losses on chromosomes 10 and 14 were associated with distinct expression profiles, including increased expression of several genes related to the insulin-like growth factor (IGF) (IGF2, IGFBP3 and AKT3) or wingless (WNT) (CTNNB1, CDK5R1, ENC1 and CCND1) pathways. Taken together, our microarray-based expression profiling revealed interesting novel candidate genes and pathways that may contribute to meningioma progression. (C) 2004 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 15540215
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  • 6
    Keywords: APOPTOSIS ; CANCER ; EXPRESSION ; CELL ; Germany ; human ; IN-VIVO ; KINASE ; MODEL ; VIVO ; GENE ; GENE-EXPRESSION ; GENES ; HYBRIDIZATION ; PROTEIN ; RNA ; METABOLISM ; cell line ; LINES ; MICE ; DNA ; CARCINOGENESIS ; animals ; KERATINOCYTES ; SKIN ; BIOLOGY ; cell cycle ; CELL-CYCLE ; CELL-LINES ; CYCLE ; DOWN-REGULATION ; MOUSE ; IDENTIFICATION ; IN-SITU ; PROGRESSION ; MALIGNANCIES ; gene expression ; EXPRESSION ANALYSIS ; HUMANS ; DESIGN ; UP-REGULATION ; MOUSE SKIN ; skin carcinogenesis ; genetics ; statistics ; CELL-LINE ; LINE ; ADHESION ; CELL-ADHESION ; ONCOGENE ; INVOLVEMENT ; RT-PCR ; KINETICS ; cell lines ; heredity ; SKIN-CANCER ; HUMAN SKIN ; in situ hybridization ; MALIGNANCY ; ONCOLOGY ; ANNOTATION ; ENHANCED EXPRESSION ; cell adhesion ; LEVEL ; analysis ; CANCER DEVELOPMENT ; cluster analysis ; S100A8 ; MAP ; in vivo ; RELEVANCE ; Oligonucleotide Array Sequence Analysis ; SPECIMENS ; animal ; Carcinoma,Squamous Cell ; SQUAMOUS-CELL ; SET ; animal model ; molecular genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Skin Neoplasms ; Cell Line,Tumor ; cytology ; DNA,Complementary ; epithelial skin cancer ; Gene Expression Regulation,Neoplastic ; HUMAN-SKIN ; Microscopy,Fluorescence ; Protein-Serine-Threonine Kinases ; RNA,Messenger ; tumour specimen
    Abstract: Chemically induced mouse skin carcinogenesis represents the most extensively utilized animal model to unravel the multistage nature of tumour development and to design novel therapeutic concepts of human epithelial neoplasia. We combined this tumour model with comprehensive gene expression analysis and could identify a large set of novel tumour-associated genes that have not been associated with epithelial skin cancer development yet. Expression data of selected genes were confirmed by semiquantitative and quantitative RT-PCR as well as in situ hybridization and immunofluorescence analysis on mouse tumour sections. Enhanced expression of genes identified in our screen was also demonstrated in mouse keratinocyte cell lines that form tumours in vivo. Self-organizing map clustering was performed to identify different kinetics of gene expression and coregulation during skin cancer progression. Detailed analysis of differential expressed genes according to their functional annotation confirmed the involvement of several biological processes, such as regulation of cell cycle, apoptosis, extracellular proteolysis and cell adhesion, during skin malignancy. Finally, we detected high transcript levels of ANXA1, LCN2 and S100A8 as well as reduced levels for NDR2 protein in human skin tumour specimens demonstrating that tumour-associated genes identified in the chemically induced tumour model might be of great relevance for the understanding of human epithelial malignancies as well
    Type of Publication: Journal article published
    PubMed ID: 16247483
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  • 7
    Keywords: EXPRESSION ; GROWTH ; IN-VITRO ; evaluation ; Germany ; IN-VIVO ; VIVO ; CDNA ; CLONES ; GENE ; GENE-EXPRESSION ; GENES ; microarray ; transcription ; TISSUE ; RELEASE ; NF-KAPPA-B ; INJURIES ; MECHANISM ; TRANSCRIPTION FACTOR ; AP-1 ; KERATINOCYTES ; mechanisms ; SKIN ; C-JUN ; fibroblasts ; SIGNAL ; TARGET ; IDENTIFICATION ; gene expression ; SUBUNIT ; REPAIR ; WILD-TYPE ; Jun ; SUBUNITS ; GROWTH-FACTOR-BETA ; DIFFERENTIAL EXPRESSION ; expression profiling ; DISSECTION ; SECTIONS ; INJURY ; CDNA MICROARRAY ; MOLECULAR-MECHANISM ; fibroblast ; mesenchyme ; GLUCOCORTICOID-TREATED MICE ; MOUSE DEVELOPMENT ; SKIN FRAGILITY
    Abstract: Mesenchymal - epithelial interactions are increasingly considered to be of vital importance for epithelial homeostasis and regeneration. In skin, the transcription factor AP-1 was shown to be critically involved in the communication between keratinocytes and dermal. broblasts. After skin injury, the release of IL-1 from keratinocytes induces the activity of the AP-1 subunits c-Jun and JunB in. broblasts leading to a global change in gene expression. To identify AP-1 target genes in. broblasts, which are involved in the process of cutaneous repair, we performed gene expression pro. ling of wild-type, c-jun- and junB-deficient. broblasts in response to IL-1, mimicking the initial phase of wound healing. Using a 15K cDNA collection, over 1000 genes were found to be Jun-dependent and additional 300 clones showed IL-1 responsiveness. Combinatorial evaluation allowed for the dissection of the specific contribution of either AP-1 subunit to gene regulation. Besides previously identified genes that are involved in cutaneous repair, we have identified novel genes regulated during wound healing in vivo and showed their expression by. broblasts on wound sections. The identification of novel Jun target genes should provide a basis for understanding the molecular mechanisms underlying mesenchymal - epithelial interactions and the critical contribution of AP-1 to tissue homeostasis and repair
    Type of Publication: Journal article published
    PubMed ID: 15273721
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  • 8
    Keywords: CANCER ; CELLS ; EXPRESSION ; tumor ; CELL ; Germany ; CLASSIFICATION ; RISK ; CDNA ; DISTINCT ; GENE ; GENE-EXPRESSION ; GENES ; microarray ; PROTEIN ; PROTEINS ; RNA ; SAMPLE ; SAMPLES ; PATIENT ; MECHANISM ; INDUCTION ; CELL-CYCLE ; CYCLE ; chromosome ; IDENTIFICATION ; cytogenetics ; gene expression ; leukemia ; ABERRATIONS ; INSTABILITY ; TRANSFORMATION ; DUPLICATION ; REPLICATION ; OVEREXPRESSION ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; MITOSIS ; BOUNDARY ; CDK2-CYCLIN ; centrosome aberrations,aneuploidy,numerical chromosome changes,acute myeloid leukemia
    Abstract: Centrosomes, which mediate accurate chromosome segregation during mitosis, undergo duplication precisely once per cell division at the G(1)/S boundary. Recently, we described centrosome aberrations as a possible cause of aneuploidy in acute myeloid leukemia (AML) and found a correlation of the percentage of cells carrying abnormal centrosomes to their cytogenetic risk pro. le. To elucidate the molecular events responsible for the development of centrosome aberrations in AML, tumor RNA of 29 AML samples was hybridized to cDNA microarrays. The microarrays comprised some 2800 different genes with relevance to hematopoiesis, tumorigenesis and mitosis and included a set of 359 centrosome-associated genes. We identified two gene expression signatures, which allowed an accurate classification according to the extent of centrosome aberrations and the ploidy status in 28 of 29 patients each. Specifically, 18 genes were present in both signatures, including genes that code for cell cycle regulatory proteins (cyclin A2, cyclin D3, cyclin H, CDK6, p18(INK4c), p21(Cip1), PAK1) and centrosome-associated proteins ( pericentrin, alpha2-tubulin, NUMA1, TUBGCP2, PRKAR2A). In conclusion, the high expression of centrosome-associated genes matches the description of centrosome aberrations in several tumor types. Moreover, in AML the identification of G(1)/S-phase stimulatory genes suggests that one mechanism of aneuploidy induction might be the deregulation of centrosome replication at the G(1)/S boundary
    Type of Publication: Journal article published
    PubMed ID: 14767474
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  • 9
    Keywords: CANCER ; EXPRESSION ; IRRADIATION ; proliferation ; SURVIVAL ; tumor ; CELL ; CELL-PROLIFERATION ; COMBINATION ; Germany ; neoplasms ; THERAPY ; COMMON ; screening ; SYSTEM ; GENE ; GENE-EXPRESSION ; GENES ; HYBRIDIZATION ; microarray ; transcription ; TISSUE ; TUMORS ; SURGERY ; STAGE ; IDENTIFICATION ; IN-SITU ; COMPARATIVE GENOMIC HYBRIDIZATION ; immunohistochemistry ; MALIGNANCIES ; gene expression ; NUMBER ; AGE ; RATES ; chemotherapy ; LINE ; BLADDER-CANCER ; MARKERS ; p53 ; PROGNOSTIC-FACTORS ; RESECTION ; PARAMETERS ; CENTRAL-NERVOUS-SYSTEM ; CANCER-RESEARCH ; SERIES ; FLUORESCENCE ; PROGNOSTIC FACTOR ; MITOSIS ; CHILDHOOD ; GRADE ; CYTOGENETIC ANALYSIS ; GENE-EXPRESSION PATTERNS ; KINASE GENE ; PRIMITIVE NEUROECTODERMAL TUMORS
    Abstract: Medulloblastoma, a primitive neuroectodermal tumor of the cerebellum, is one of the most common central nervous system malignancies of childhood. Despite aggressive multimodal therapy, including surgery, irradiation, and chemotherapy, 5-year survival rates have only approached 50-60%. To identify potential candidate genes that predict for overall survival (OS), we performed a gene expression profiling analysis in 35 newly diagnosed medulloblastoma neoplasms. Subsequently, the nine most promising candidate genes were analyzed by immunohistochemistry and fluorescence in situ hybridization on tumor tissue microarrays representing a series of 180 tumors. We found 54 genes in which expression levels predicted for unfavorable survival in medulloblastoma. In line with the gene expression profiling analysis, a positive staining for STK15 (P = 0.0006), stathmin 1 (P = 0.001), and cyclin D1 (P = 0.03) was associated with an unfavorable OS, whereas cyclin B1, DAXX, Ki-67, MYC, NRAS. and p53 showed no statistical significant effect. In compar- ison to clinically defined parameters such as gender, age, metastatic stage, extent of tumor resection, application of chemotherapy, and tumor grade, positive staining for STK15 was identified as an independent prognostic factor for OS (P = 0.026). Moreover, additional gene copy numbers of MYC (P = 0.003) and STK15 (P = 0.05) predicted for poor survival. The combination of gene expression profiling with tissue microarray experiments allowed the identification of a series of candidate genes that predicts for survival in medulloblastoma. Of the results highlighted by the various data analysis procedures, genes associated with cell proliferation (cyclin D1), transcription (MYC), and especially mitosis (stathmin 1, STK15) appear particularly intriguing with respect to medulloblastoma pathomechanism
    Type of Publication: Journal article published
    PubMed ID: 15126347
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  • 10
    Keywords: EXPRESSION ; Germany ; PROTEIN ; MESSENGER-RNA EXPRESSION ; MARKER ; NERVOUS-SYSTEM ; gene amplification ; expression profiling ; protein expression ; RE ; PRIMITIVE NEUROECTODERMAL TUMORS ; CLINICAL-RELEVANCE ; PROGNOSTIC MARKER ; CHILDHOOD MEDULLOBLASTOMA ; DEPENDENT KINASE 6 ; HYBRIDIZATION DETECTS ; PEDIATRIC-ONCOLOGY-GROUP ; RISK STRATIFICATION
    Type of Publication: Journal article published
    PubMed ID: 16314645
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