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  • IDENTIFICATION  (40)
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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: 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: RECEPTOR ; CANCER ; EXPRESSION ; tumor ; carcinoma ; Germany ; GENE ; GENES ; HYBRIDIZATION ; microarray ; DNA ; ASSOCIATION ; BREAST-CANCER ; IDENTIFICATION ; IN-SITU ; COPY NUMBER ; microarrays ; DESIGN ; NUMBER ; ABERRATIONS ; REGIONS ; OVEREXPRESSION ; CLUSTER ; E-cadherin ; RE ; CANDIDATE GENES ; REVERSE TRANSCRIPTION-PCR ; EXPRESSION PATTERNS ; ARRAY-CGH ; LOBULAR CARCINOMA
    Abstract: Purpose: Invasive ductal carcinoma and invasive lobular carcinoma (ILC) represent the major histologic subtypes of invasive breast cancer. They differ with regard to presentation, metastatic spread, and epidemiologic features. To elucidate the genetic basis of these differences, we analyzed copy number imbalances that differentiate the histologic subtypes. Experimental Design: High-resolution genomic profiling of 40 invasive breast cancers using matrix-comparative genomic hybridization with an average resolution of 0.5 Mb was conducted on bacterial artificial chromosome microarrays. The data were subjected to classification and unsupervised hierarchical cluster analyses. Expression of candidate genes was analyzed in tumor samples. Results: The highest discriminating power was achieved when combining the aberration patterns of chromosome arms 1q and 16p, which were significantly more often gained in ILC. These regions were further narrowed down to subregions 1q24.2-25.1, 1q25.3-q31.3, and 16p11.2. Located within the candidate gains on 1q are two genes, FMO2 and PTGS2, known to be overexpressed in ILC relative to invasive ductal carcinoma. Assessment of four candidate genes on 16p11.2 by real-time quantitative PCR revealed significant overexpression of FUS and ITGAX in ILC with 16p copy number gain. Unsupervised hierarchical cluster analysis identified three molecular subgroups that are characterized by different aberration patterns, in particular concerning gain of MYC (8q24) and the identified candidate regions on 1q24.2-25.1, 1q25.3-q31.3, and 16p11.2. These genetic subgroups differed with regard to histology, tumor grading, frequency of alterations, and estrogen receptor expression. Conclusions: Molecular profiling using bacterial artificial chromosome arrays identified DNA copy number imbalances on 1q and 16p as significant classifiers of histologic and molecular subgroups
    Type of Publication: Journal article published
    PubMed ID: 16428471
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  • 4
    Keywords: CELLS ; EXPRESSION ; CELL ; human ; INFORMATION ; SYSTEM ; SYSTEMS ; TOOL ; GENE-EXPRESSION ; GENOME ; RNA ; TISSUE ; TISSUES ; BIOLOGY ; MOLECULAR-BIOLOGY ; SEQUENCE ; SEQUENCES ; MATURATION ; TARGET ; IDENTIFICATION ; PATTERNS ; DIFFERENCE ; STABILITY ; Jun ; TARGETS ; FUTURE ; HEMATOPOIETIC-CELLS ; LOCATION ; POSTTRANSCRIPTIONAL REGULATION ; molecular biology ; molecular ; PATTERN ; LIBRARIES ; C-ELEGANS ; LINEAGE ; TRANSLATION ; analysis ; PROFILES ; EXPRESSION PROFILES ; rodents ; USA ; CAENORHABDITIS-ELEGANS/ ; UNIT ; PRECURSOR ; TOOLS ; SET ; MENTAL-RETARDATION PROTEIN ; MicroRNAs ; ZEBRAFISH ; MICRORNA ; miRNAs ; ANIMAL DEVELOPMENT
    Abstract: MicroRNAs (miRNAs) are small noncoding regulatory RNAs that reduce stability and/or translation of fully or partially sequence-complementary target mRNAs. In order to identify miRNAs and to assess their expression patterns, we sequenced over 250 small RNA libraries from 26 different organ systems and cell types of human and rodents that were enriched in neuronal as well as normal and malignant hematopoietic cells and tissues. We present expression profiles derived from clone count data and provide computational tools for their analysis. Unexpectedly, a relatively small set of miRNAs, many of which are ubiquitously expressed, account for most of the differences in miRNA profiles between cell lineages and tissues. This broad survey also provides detailed and accurate information about mature sequences, precursors, genome locations, maturation processes, inferred transcriptional units, and conservation patterns. We also propose a subclassification scheme for miRNAs for assisting future experimental and computational functional analyses
    Type of Publication: Journal article published
    PubMed ID: 17604727
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  • 5
    Keywords: brain ; EXPRESSION ; tumor ; Germany ; human ; DISTINCT ; GENE ; GENES ; microarray ; TUMORS ; DNA ; primary ; IDENTIFICATION ; DIFFERENCE ; MUTATION ; LINE ; ABERRATIONS ; pathology ; expression profiling ; METHYLATION ; ASTROCYTOMAS ; GLIOMAS ; LOH ; HYPERMETHYLATION ; CDNA MICROARRAY ; neuroblastoma ; molecular ; aberrant expression ; TUMOR-SUPPRESSOR ; SUPPRESSOR GENE ; GLIOMA ; HUMAN GLIOMAS ; analysis ; SUPPRESSOR ; MOLECULAR-GENETICS ; PROFILES ; LOSSES ; OLIGODENDROGLIAL TUMORS ; CANDIDATE ; UNIT ; GLIOBLASTOMA ; MULTIPLE GENES ; aberration ; SECONDARY GLIOBLASTOMAS ; CDNA-MICROARRAY ; PHASE-III TRIAL ; 19Q LOSS ; CANDIDATE TUMOR-SUPPRESSOR
    Abstract: Allelic losses on 19q are found in the majority of oligodendroglial tumors and approximately one-third of diffuse astrocytomas. However, the tumor suppressor genes (TSG) on 19q are still elusive. Using cDNA microarray expression profiling, EMP3 at 19q13.3 was among those genes showing the most pronounced expression differences. In line with this, other authors reported EMP3 as being epigenetically silenced in neuroblastomas and astrocytomas. To further investigate EMP3 as a TSG candidate on 19q13.3, we performed molecular analysis of this gene in 162 human gliomas. Mutation analysis did not reveal EMP3 alteration in 132 gliomas. In oligodendroglial tumors, we found that aberrant methylation in the 5'-region of EMP3 was significantly associated with reduced mRNA expression and LOH 19q. In astrocytomas, EMP3 hypermethylation was also paralleled by reduced expression but was independent of the 19q status. EMP3 hypermethylation was detected in more than 80% of diffuse, anaplastic astrocytomas and secondary glioblastomas. Primary glioblastomas, however, mostly lacked EMP3 hypermethylation and frequently overexpressed EMP3. Our data corroborate that oligodendroglial and astrocytic gliomas often show EMP3 hypermethylation and aberrant expression. Furthermore, our findings suggest that primary and secondary glioblastomas are not only characterized by distinct genetic profiles but also differ in their epigenetic aberrations
    Type of Publication: Journal article published
    PubMed ID: 17610521
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  • 6
    Keywords: EXPRESSION ; tumor ; IDENTIFICATION ; PROGRESSION ; OVARIAN-CANCER ; PROGNOSTIC-FACTORS ; CHILDHOOD MEDULLOBLASTOMA ; STEM-CELL ; BREAST-CANCER CELLS ; INFLUENCES ZYXIN LOCALIZATION
    Abstract: Medulloblastoma is the most common malignant pediatric brain tumor and is one of the leading causes of cancer-related mortality in children. Treatment failure mainly occurs in children harboring metastatic tumors, which typically carry an isochromosome 17 or gain of 17q, a common hallmark of intermediate and high-risk medulloblastoma. Through mRNA expression profiling, we identified LIM and SH3 protein 1 (LASP1) as one of the most upregulated genes on chromosome 17q in tumors with 17q gain. In an independent validation cohort of 101 medulloblastoma samples, the abundance of LASP1 mRNA was significantly associated with 17q gain, metastatic dissemination, and unfavorable outcome. LASP1 protein expression was analyzed by immunohistochemistry in a large cohort of patients (n = 207), and high protein expression levels were found to be strongly correlated with 17q gain, metastatic dissemination, and inferior overall and progression-free survival. In vitro experiments in medulloblastoma cell lines showed a strong reduction of cell migration, increased adhesion, and decreased proliferation upon LASP1 knockdown by small interfering RNA-mediated silencing, further indicating a functional role for LASP1 in the progression and metastatic dissemination of medulloblastoma.
    Type of Publication: Journal article published
    PubMed ID: 20924110
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  • 7
    Keywords: CANCER ; EXPRESSION ; QUANTIFICATION ; IDENTIFICATION ; AMINO-ACIDS ; POSTTRANSCRIPTIONAL REGULATION ; MESSENGER-RNAS ; BIOGENESIS ; TRANSLATION INITIATION ; CELL-CULTURE ; MICRORNA-BINDING-SITES
    Abstract: Background: MicroRNAs are 22 nucleotides long non-coding RNAs and exert their function either by transcriptional or translational inhibition. Although many microRNA profiles in different tissues and disease states have already been discovered, only little is known about their target proteins. The microRNA miR-155 is deregulated in many diseases, including cancer, where it might function as an oncoMir. Methodology/Principal Findings: We employed a proteomics technique called "stable isotope labelling by amino acids in cell culture" (SILAC) allowing relative quantification to reliably identify target proteins of miR-155. Using SILAC, we identified 46 putative miR-155 target proteins, some of which were previously reported. With luciferase reporter assays, CKAP5 was confirmed as a new target of miR-155. Functional annotation of miR-155 target proteins pointed to a role in cell cycle regulation. Conclusions/Significance: To the best of our knowledge we have investigated for the first time miR-155 target proteins in the HEK293T cell line in large scale. In addition, by comparing our results to previously identified miR-155 target proteins in other cell lines, we provided further evidence for the cell line specificity of microRNAs
    Type of Publication: Journal article published
    PubMed ID: 21799781
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  • 8
    Keywords: CANCER ; EXPRESSION ; GROWTH ; transcription ; IDENTIFICATION ; GLIOMA ; MOUSE MODELS ; TLX ; NUCLEAR RECEPTOR TAILLESS ; GLIOMAGENESIS
    Abstract: Cancer stem cells (CSCs) have been suggested as potential therapeutic targets for treating malignant tumors, but the in vivo supporting evidence is still missing. Using a GFP reporter driven by the promoter of the nuclear receptor tailless (Tlx), we demonstrate that Tlx(+) cells in primary brain tumors are mostly quiescent. Lineage tracing demonstrates that single Tlx(+) cells can self-renew and generate Tlx(-) tumor cells in primary tumors, suggesting that they are brain tumor stem cells (BTSCs). After introducing a BTSC-specific knock-out of the Tlx gene in primary mouse tumors, we observed a loss of self-renewal of BTSCs and prolongation of animal survival, accompanied by induction of essential signaling pathways mediating cell-cycle arrest, cell death, and neural differentiation. Our study demonstrates the feasibility of targeting glioblastomas and indicates the suitability of BTSCs as therapeutic targets, thereby supporting the CSC hypothesis.
    Type of Publication: Journal article published
    PubMed ID: 24835569
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  • 9
    Keywords: CELLS ; EXPRESSION ; GROWTH ; PATHWAY ; BIOMARKERS ; IDENTIFICATION ; LIGAND-BINDING DOMAIN ; ESTROGEN-RELATED-RECEPTOR ; TRANSCRIPTIONAL ACTIVITIES ; ENDOCRINE RESISTANCE
    Abstract: Endocrine treatment regimens for breast cancer that target the estrogen receptor-alpha (ER alpha) are effective, but acquired resistance remains a limiting drawback. One mechanism of acquired resistance that has been hypothesized is functional substitution of the orphan receptor estrogen-related receptor-alpha (ERR alpha) for ER alpha. To examine this hypothesis, we analyzed ERR alpha and ER alpha in recurrent tamoxifen-resistant breast tumors and conducted a genome-wide target gene profiling analysis of MCF-7 breast cancer cell populations that were sensitive or resistant to tamoxifen treatment. This analysis uncovered a global redirection in the target genes controlled by ER alpha, ERR alpha, and their coactivator AIB1, defining a novel set of target genes in tamoxifen-resistant cells. Beyond differences in the ER alpha and ERR alpha target gene repertoires, both factors were engaged in similar pathobiologic processes relevant to acquired resistance. Functional analyses confirmed a requirement for ERR alpha in tamoxifen-and fulvestrant-resistant MCF-7 cells, with pharmacologic inhibition of ERR alpha sufficient to partly restore sensitivity to antiestrogens. In clinical specimens (n - 1041), increased expression of ERR alpha was associated with enhanced proliferation and aggressive disease parameters, including increased levels of p53 in ER alpha-positive cases. In addition, increased ERR alpha expression was linked to reduced overall survival in independent tamoxifen-treated patient cohorts. Taken together, our results suggest that ER alpha and ERR alpha cooperate to promote endocrine resistance, and they provide a rationale for the exploration of ERR alpha as a candidate drug target to treat endocrine-resistant breast cancer.
    Type of Publication: Journal article published
    PubMed ID: 25643697
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  • 10
    Keywords: CANCER ; CELLS ; EXPRESSION ; GROWTH ; carcinoma ; GENE ; GENE-EXPRESSION ; GENES ; microarray ; PROTEIN ; SAMPLE ; SAMPLES ; murine ; AP-1 ; CARCINOGENESIS ; tumour ; SKIN ; MOUSE ; TRANSCRIPTION FACTORS ; IDENTIFICATION ; PROGRESSION ; gene expression ; PROMOTERS ; skin carcinogenesis ; METASTASIS ; SSH ; PCR ; TRANSFORMATION ; EPITHELIAL-CELLS ; squamous cell carcinoma ; FRAGMENTS ; MULTISTAGE CARCINOGENESIS ; real-time PCR ; expression profiling ; PHORBOL ESTER ; CDNA MICROARRAY ; NMRI MOUSE SKIN ; tumour promoter
    Abstract: Malignant transformation of mouse skin by chemical carcinogens and tumour promoters, such as the phorbol ester 12-O- tetradecanoylphorbol-13-acetate (TPA), is a multi-stage process that leads to squamous cell carcinoma (SCC) formation. In an effort to identify turnour-associated genes, we studied the influence of short-term TPA-treatment on the gene expression profile of murine skin. A comprehensive microarray with some 5,000 murine gene specific cDNA fragments was established and hybridised with pooled RNA derived from control and TPA-treated dorsal skin samples. Of these genes, 54 were up- and 35 were down-regulated upon TPA application. Additionally, we performed suppression subtractive hybridisation (SSH) with respective RNA pools to generate and analyse a cDNA library enriched for TPA- inducible genes. Expression data of selected genes were confirmed by quantitative real-time PCR and Northern blot analysis. Comparison of microarray and SSH data revealed that 26% of up-regulated genes identified by expression profiling matched with those present in the SSH library. Besides numerous known genes, we identified a large set of unknown cDNAs that represent previously unrecognised TPA-regulated genes in murine skin with potential function in tumour promotion. Additionally, some TPA-induced genes, such as SprrIA, Saa3, junB, II4ralpha, Gp38, RalGDS and Slpi exhibit high basal level in advanced stages of skin carcinogenesis, suggesting that at least a subgroup of the identified TPA-regulated genes may contribute to tumour progression and metastasis. (C) 2003 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 12640676
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