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  • TUMORS  (37)
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  • 2
    Keywords: EXPRESSION ; tumor ; carcinoma ; CELL ; Germany ; TYROSINE KINASE ; screening ; SITE ; SITES ; DISTINCT ; microarray ; PROTEIN ; TISSUE ; TUMORS ; primary ; GROWTH-FACTOR RECEPTOR ; FREQUENCY ; FREQUENCIES ; STAGE ; PROGRESSION ; immunohistochemistry ; ABERRATIONS ; HEAD ; ONCOPROTEIN ; CARCINOMAS ; NECK ; squamous cell carcinoma ; GREECE ; gene amplification ; head and neck ; laryngeal carcinoma ; OROPHARYNGEAL ; C-MYC ; CANCER PATIENTS ; CYCLIN D1 OVEREXPRESSION ; cytogenetic aberration ; head and neck squamous cell carcinoma (HNSCC) ; immunohistochemistry (IHC) ; MICROARRAY ANALYSIS ; oncoprotein overexpression ; OVEREXPRESSION ; POOR-PROGNOSIS ; tissue microarray (TMA) ; tumor classification
    Abstract: Background: Tissue microarray (TMA) analysis is a high-throughput approach that allows the screening of large tumor collectives for cytogenetic aberrations. In this study, a TMA of a large collection of clinically well-defined primary squamous cell carcinomas of the head and neck (HNSCC) was used to determine the expression of several oncoproteins. Materials and Methods: A TMA containing 547 primary HNSCC was used for the analysis of cyclinD1, c-myc, erbb1 and erbb2 expression by immunohistochemistry (IHC). Results: CyclinD1 and c-myc were overexpressed at higher frequencies in primary pharyngeal and laryngeal carcinomas compared with primary oral carcinomas (p 〈 0.001 and p 〈 0.001), while erbb1 and erbb2 overexpression was associated with oral site (p 〈 0.001 and p = 0.04, respectively). Furthermore, cyclinD1 overexpression correlated with stage IV primary carcinomas (p = 0.04). Conclusion: HNSCC is a heterogenous group of tumors, which, depending on anatomic sites and clinical stage, shows variable expressions of the oncoproteins described. This indicates a specific pathogenic role of these oncoproteins in different subtypes of HNSCC and may have therapeutic implications
    Type of Publication: Journal article published
    PubMed ID: 14666705
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  • 3
    Keywords: SPECTRA ; CANCER ; tumor ; CELL ; Germany ; DISEASE ; NEW-YORK ; CLONES ; GENE ; HYBRIDIZATION ; cell line ; TUMORS ; LINES ; primary ; CELL-LINES ; chromosome ; IN-SITU ; AMPLIFICATION ; chromosome 2 ; COMPARATIVE GENOMIC HYBRIDIZATION ; COPY NUMBER ; COPY-NUMBER ; LYMPHOMA ; ABERRATIONS ; FISH ; REGIONS ; ONCOGENE ; SEGMENTS ; FLUORESCENCE ; IMBALANCES ; cytogenetic aberration ; fluorescence in situ hybridization ; Hodgkin's lymphoma ; JAK2 ; JUMPING TRANSLOCATIONS ; REL ; telomeric segment translocation ; YAC
    Abstract: Four Hodgkin's lymphoma cell lines (KM-H2, HDLM-2, L428, L1236) were analyzed for cytogenetic aberrations, applying multiplex fluorescence in situ hybridization, chromosome banding and comparative genomic hybridization. Each line was characterized by a highly heterogeneous pattern of karyotypic changes with a large spectrum of different translocated chromosomes (range 22- 57). A recurrent finding in all cell lines was the presence of chromosomal rearrangements of the short arm of chromosome 2 involving the REL oncogene locus. Furthermore, multiple translocated copies of telomeric chromosomal segments were frequently detected. This resulted in a copy number increase of putative oncogenes, e.g., JAK2 (9p24) in 3 cell lines, FGFR3 (4p16) and CCND2 (12p13) in 2 cell lines as well as MYC (8q24) in I cell line. Our data confirm previous cytogenetic results from primary Hodgkin's tumors suggesting an important pathogenic role of REL and JAK2 in this disease. In addition, they provide evidence for a novel cytogenetic pathomechanism leading to increased copy numbers of putative oncogenes from terminal chromosomal regions, most probably in the course of chromosomal stabilization by telomeric capture. (C) 2002 Wiley- Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 12478664
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  • 4
    Keywords: EXPRESSION ; INHIBITOR ; tumor ; carcinoma ; Germany ; KINASE ; TYROSINE KINASE ; GENE ; HYBRIDIZATION ; microarray ; PROTEIN ; TISSUE ; TUMORS ; TYROSINE KINASE INHIBITOR ; IN-SITU ; immunohistochemistry ; NUMBER ; PATHOGENESIS ; FISH ; MUTATIONS ; SQUAMOUS-CELL CARCINOMA ; HEAD ; NECK ; PREVALENCE ; FLUORESCENCE ; OVEREXPRESSION ; imatinib ; fluorescence in situ hybridization ; GAINS ; C-KIT ; ADENOID CYSTIC CARCINOMA ; GASTROINTESTINAL STROMAL TUMORS ; INHIBITORS ; in situ hybridization ; salivary gland tumor ; AMPLIFICATIONS ; GLAND ; intensity ; SUBTYPE ; TUMOR TISSUE ; KINASE INHIBITORS ; SUBTYPES ; KIT ; tissue microarray ; tissue microarray analysis
    Abstract: Adenoid cystic carcinoma (ACC) of the salivary gland is characterized by a prolonged but inevitably unfavorable clinical course. Recent studies suggested the transmembrane tyrosine kinase KIT to be involved in ACC pathogenesis. To investigate KIT expression in histologically defined subgroups of ACC and to clarify whether KIT gene copy number gain contributes to KIT overexpression, tumor tissue microarray sections including 55 ACC tumors were analyzed by fluorescence in situ hybridization (FISH) and immunohistochemistry (IHC). The prevalence of positive KIT immunostaining was 89% (49/55). Strong immunostaining of KIT was only found in cribriform and tubular but never in solid subtypes (p = 0.02). Average KIT staining intensity was higher in cribriform and tubular (n = 37) compared to solid (n = 18) ACC subtypes (p = 0.005). FISH analysis revealed copy number gains of the KIT gene in 6.1% (3/49) of tumors analyzed. Our results implicate that specific KIT tyrosine kinase inhibitors such as imatinib, might be used in future therapeutic approaches against subgroups of ACC. (c) 2005 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16054424
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  • 5
    Keywords: EXPRESSION ; tumor ; carcinoma ; Germany ; GENE ; GENES ; HYBRIDIZATION ; microarray ; PROTEIN ; TISSUE ; TUMORS ; DNA ; PROGRESSION ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; microarrays ; HEAD ; NECK ; squamous cell carcinoma ; PROGNOSTIC VALUE ; CYCLIN D1 OVEREXPRESSION ; OVEREXPRESSION ; POOR-PROGNOSIS ; CHROMOSOMAL IMBALANCES ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; CANDIDATE GENES ; tissue microarray analysis ; SPECIMENS ; ARRAY CGH
    Abstract: Chromosomal band 11q13 is frequently amplified in oral squamous cell carcinoma (OSCC) and assumed to be critically involved in tumor initiation and progression by proto-oncogene activation. Though cyclin D1 (CCND1) is supposed to be the most relevant oncogene, several additional putative candidate genes are inside this chromosomal region, for which their actual role in tumorigenesis still needs to be elucidated. To characterize the 11q13 amplicon in detail, 40 OSCCs were analyzed by comparative genomic hybridization to DNA microarrays (matrix-CGH) containing BAC clones derived from chromosomal band 11q13. This high-resolution approach revealed a consistent amplicon about 1.7 Mb in size including the CCND1 oncogene. Seven BAC clones covering FGF3, EMS1, and SHANK2 were shown to be frequently coamplified inside the CCND1 amplicon. Subsequent analysis of tissue microarrays; by FISH revealed amplification frequencies of 36.8% (88/239) for CCND1, 34.3% (60/ 175) for FGF3, 37.4% (68/182) for EMS1, and 36.3% (61/168) for SHANK2. Finally, quantitative mRNA expression analysis demonstrated consistent overexpression of CCND1 in all tumors and of EMS1 and SHANK2 in a subset of specimens with 11q13 amplification, but no expression of FGF3 in any of the cases. Our study underlines the critical role of CCND1 in OSCC development and additionally points to the functionally related genes EMS1 and SHANK2, both encoding for cytoskeleton-associated proteins, which are frequently coamplified with CCND1 and therefore could cooperatively contribute to OSCC pathogenesis. (c) 2005 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16235239
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  • 6
    Keywords: EXPRESSION ; GROWTH ; proliferation ; carcinoma ; Germany ; INHIBITION ; PATHWAY ; DISTINCT ; GENE ; GENES ; microarray ; PROTEIN ; DIFFERENTIATION ; TISSUE ; TUMORS ; SKIN ; IN-SITU ; AMPLIFICATION ; COPY NUMBER ; immunohistochemistry ; NUMBER ; MUTATIONS ; ONCOGENE ; HUMAN HOMOLOG ; HEAD ; PREVALENCE ; PRECURSORS ; EFFECTOR ; basal cell carcinoma ; N-MYC ; CELL CARCINOMA ; SUBSET ; fluorescence in situ hybridisation ; LOCUS ; tissue microarray ; NMYC ; HUMAN NEUROBLASTOMA ; SPECIMENS
    Abstract: Formation of basal cell carcinoma (BCC) has been linked to deregulation in the sonic hedgehogh (Shh) signalling pathway. Though mutations of the genes, PTCHI and SMO, are known to be involved in aberrant Shh signalling, the distinct downstream effectors of these genes are poorly described. Studies have indicated that the NMYC oncogene is a potential Shh downstream effector. To assess the expression of Nmyc protein and gene copy numbers of the NMYC gene locus in a representative BCC tumour collection, immunohistochemistry (IHC) and fluorescence in situ hybridisation (FISH) were performed on 273 BCC specimens of different growth patterns and anatomic localisations on tissue microarray (TMA) sections. High Nmyc protein expression was detected in 72.7% (160/220) of all BCC specimens. Strong Nmyc immunopositivity was more frequently found in infiltrative BCCs compared to nodular/superficial BCCs (p=0.005), and in BCCs of the head compared to BCCs of other anatomic localisations (p=0.021). The prevalence of NMYC copy number gains was 17.5% (37/211), including three tumours with nodular differentiation that exhibited a distinct high-level amplification of the NMYC locus. These data indicate that high expression of the Shh downstream mediator, Nmyc, is a frequent event in BCC, predominantly in more aggressive subtypes. Although the NMYC copy number gain found in a subset of cases might contribute to this aberrant Nmyc protein expression by a gene dosage effect, our data suggests that Nmyc protein can also be induced by aberrant Shh signalling, acting as an effector molecule of the Shh pathway. Novel systemic anti-sense NMYC inhibition strategies could be a promising option for therapy-refractory BCC
    Type of Publication: Journal article published
    PubMed ID: 16596176
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  • 7
    Keywords: EXPRESSION ; tumor ; carcinoma ; CELL ; Germany ; human ; INFORMATION ; HEPATOCELLULAR-CARCINOMA ; HISTORY ; GENE ; GENES ; HYBRIDIZATION ; DIFFERENTIATION ; TUMORS ; RESOLUTION ; DNA ; MECHANISM ; mechanisms ; ADENOMAS ; hepatocellular carcinoma ; PROGRESSION ; COMPARATIVE GENOMIC HYBRIDIZATION ; COPY NUMBER ; NUMBER ; CHROMOSOMAL-ABERRATIONS ; ABERRATIONS ; IN-SITU HYBRIDIZATION ; TUMOR-SUPPRESSOR GENE ; REGION ; INSTABILITY ; REGIONS ; ONCOGENE ; TRANSFORMATION ; ORAL-CONTRACEPTIVES ; CARCINOMAS ; IMBALANCES ; CLUSTER ; MOLECULAR-MECHANISM ; TUMOR-SUPPRESSOR ; INCREASE ; CLUSTER-ANALYSIS ; CHROMOSOMAL INSTABILITY ; CHIP ; tumor suppressor gene ; cluster analysis ; LOSSES ; GLYCOGEN-STORAGE-DISEASE ; genomic ; HUMAN HEPATOCELLULAR-CARCINOMA ; ARRAY CGH ; CHROMOSOMAL-ABNORMALITIES ; TUMOR-SUPPRESSOR GENES ; ARRAY-CGH ; LIVER-CELL ADENOMAS
    Abstract: Background & Alms: To gain more information about the molecular mechanisms leading to dedifferentiation of hepatocellular adenoma (HCA) and hepatocellular carcinoma (HCC), high-resolution array-based comparative genomic hybridization (array-CGH) was performed on 24 cases of HCC and 10 cases of HCA. Methods: DNA chips containing 6251 individual bacterial artificial chromosome/plasmid artificial chromosome clones were used. They allowed for a genome-wide resolution of 1 Mb and an even higher resolution of up to 100 kb for chromosome regions recurrently involved in human tumors and for regions containing known tumor-suppressor genes and oncogenes. Results: Copy number changes on the genomic scale were found by array-based comparative genomic hybridization in all cases. In HCC, gains of chromosomal regions 1q (91.6%), and 8q (58.3%), and losses of 8p (54%) were found most frequently. Hierarchic cluster analysis branched all HCA from HCC. However, in 2 adenomas with a known history of glycogenosis type I and adenomatosis hepatis gains of 1q were found, too. The critically gained region was narrowed down to bands 1q22-23. Although no significant differences in the mean number of chromosomal aberrations were seen between adenomas and well-differentiated carcinomas (2.7 vs 4.6), a significant increase accompanied the dedifferentiation of HCC (14.1 in HCC-G2 and 16.3 in HCC-G2/3; P 〈 .02). Dedifferentiation of HCC also was correlated closely to losses of 4q and 13q (P 〈 .001 and 〈 .005, respectively). Conclusions: The increased chromosomal instability during dedifferentiation of HCC leads to an accumulation of structural chromosomal aberrations and losses and gains of defined chromosome regions
    Type of Publication: Journal article published
    PubMed ID: 16979954
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  • 8
    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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  • 9
    Keywords: APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; GROWTH ; proliferation ; tumor ; carcinoma ; CELL ; Germany ; human ; IN-VIVO ; HEPATOCELLULAR-CARCINOMA ; DISTINCT ; GENE ; GENE-EXPRESSION ; GENES ; TUMORS ; ACTIVATION ; DNA ; INFECTION ; MECHANISM ; prognosis ; mechanisms ; BREAST-CANCER ; TARGET ; virus ; TRANSGENIC MICE ; COMPARATIVE GENOMIC HYBRIDIZATION ; gene expression ; NUMBER ; etiology ; RATES ; REGION ; ONCOGENE ; ALCOHOL ; OVEREXPRESSION ; gene expression profiling ; ALCOHOL-CONSUMPTION ; CONSUMPTION ; molecular ; RE ; ARRAY ; CANDIDATE GENES ; USA ; CANDIDATE ; CANCERS ; viral ; CHROMOSOME-ABERRATIONS ; ELONGATION-FACTOR EEF1A2
    Abstract: Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide and is characterized by aggressive tumor behavior coupled with poor prognosis. Various etiologies have been linked to HCC development, most prominently chronic hepatitis B and C virus infections as well as chronic alcohol consumption. In approximately 10% of HCCs, the etiology remains cryptic; however, recent epidemiological data suggest that most of these cryptogenic HCCs develop due to nonalcoholic steatohepatitis. To identify etiology-dependent DNA copy number aberrations and genes relevant to hepatocarcinogenesis, we performed array based comparative genomic hybridization of 63 HCCs of well-defined etiology and 4 HCC cell lines followed by gene expression profiling and functional analyses of candidate genes. For a 10-megabase chromosome region on 8q24, we observed etiology-dependent copy number gains and MYC overexpression in viral and alcohol-related HCCs, resulting in up-regulation of MYC target genes. Cryptogenic HCCs showed neither 8q24 gains, nor MYC overexpression, nor target gene activation, suggesting that tumors of this etiology develop by way of a distinct MYC-independent pathomechanism. Furthermore, we detected several etiology-independent small chromosome aberrations, including amplification of MDM4 on 1q32.1 and frequent gains of EEF1A2 on 20q13.33. Both genes were overexpressed in approximately half the HCCs examined, and gene silencing reduced cell viability as well as proliferation and increased apoptosis rates in HCC cell fines. Conclusion: Our findings suggest that MDM4 and EEF1A2 act as etiology-independent oncogenes in a significant percentage of HCCs
    Type of Publication: Journal article published
    PubMed ID: 18161050
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  • 10
    Keywords: brain ; tumor ; Germany ; neoplasms ; TOOL ; HYBRIDIZATION ; DIFFERENTIATION ; TUMORS ; MARKER ; BIOLOGY ; IN-SITU ; AMPLIFICATION ; AGE ; ABERRATIONS ; FISH ; CENTRAL-NERVOUS-SYSTEM ; pathology ; CHILDREN ; BEHAVIOR ; CHROMOSOMES ; FEATURES ; brain tumor ; BRAIN-TUMORS ; PRIMITIVE NEUROECTODERMAL TUMORS ; LOCUS ; diagnostic marker ; ABUNDANT NEUROPIL ; TRUE ROSETTES ; 19q13 ; Embryonal brain tumor ; Ependymoblastoma ; ETANTR ; Molecular diagnosis ; WHO classification of CNS tumors
    Abstract: Ependymoblastoma (EBL) and embryonal tumor with abundant neuropil and true rosettes (ETANTR) are very aggressive embryonal neoplasms characterized by the presence of ependymoblastic multilayered rosettes typically occurring in children below 6 years of age. It has not been established whether these two tumors really comprise distinct entities. Earlier, using array-CGH, we identified a unique focal amplification at 19q13.42 in a case of ETANTR. In the present study, we investigated this locus by fluorescence in situ hybridization in 41 tumors, which had morphologically been diagnosed as EBL or ETANTR. Strikingly, FISH analysis revealed 19q13.42 amplifications in 37/40 samples (93%). Among tumors harboring the amplification, 19 samples were identified as ETANTR and 18 as EBL. The three remaining tumors showed a polysomy of chromosome 19. Analysis of recurrent/metastatic tumors (n = 7) showed that the proportion of nuclei carrying the amplification was increased (up to 80-100% of nuclei) in comparison to the corresponding primary tumors. In conclusion, we have identified a hallmark cytogenetic aberration occurring in virtually all embryonal brain tumors with ependymoblastic rosettes suggesting that ETANTR and EBL comprise a single biological entity. FISH analysis of the 19q13.42 locus is a very promising diagnostic tool to identify a subset of primitive neuroectodermal tumors with distinct morphology, biology, and clinical behavior
    Type of Publication: Journal article published
    PubMed ID: 20407781
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