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  • HYBRIDIZATION  (50)
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  • 1
    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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  • 2
    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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  • 3
    Keywords: tumor ; CELL ; Germany ; human ; MICROSCOPY ; SITE ; SITES ; GENE ; GENES ; HYBRIDIZATION ; PROTEIN ; PROTEINS ; DNA ; IMPACT ; image analysis ; SEQUENCE ; SEQUENCES ; chromosome ; IN-SITU ; SINGLE-COPY ; IN-SITU HYBRIDIZATION ; SURFACE ; LOCALIZATION ; MAMMALIAN-CELLS ; ONCOGENE ; UNITED-STATES ; FRAGMENTS ; FLUORESCENCE ; INTERPHASE ; SPATIAL-ORGANIZATION ; NUCLEAR-LOCALIZATION ; CHROMOSOME TERRITORIES ; INSITU HYBRIDIZATION ; ORGANIZATION ; CLUSTERS ; STATES ; CLUSTER ; DNA-SEQUENCE ; DNA-SEQUENCES ; in situ hybridization ; nuclear organization ; SUPPRESSOR GENE ; CENTROMERIC HETEROCHROMATIN ; gene loci ; heterochromatin protein 1 ; HUMAN-CHROMOSOME TERRITORIES ; INACTIVE GENES ; nontranscribed sequences ; TRANSCRIPTION SITES
    Abstract: Knowledge about the functional impact of the topological organization of DNA sequences within interphase chromosome territories is still sparse. Of the few analyzed single copy genomic DNA sequences, the majority had been found to localize preferentially at the chromosome periphery or to loop out from chromosome territories. By means of dual-color fluorescence in situ hybridization (FISH), immurrolabeling, confocal microscopy, and three-dimensional (3D) image analysis, we analyzed the intraterritorial and nuclear localization of 10 genomic fragments of different sequence classes in four different human cell types. The localization of three muscle-specific genes FLNA, NEB, and TTN, the oncogene BCL2, the tumor suppressor gene MADH4, and five putatively nontranscribed genomic sequences was predominantly in the periphery of the respective chromosome territories, independent from transcriptional status and from GC content. In interphase nuclei, the noncoding sequences were only rarely found associated with heterochromatic sites marked by the satellite III DNA D1Z1 or clusters of mammalian heterochromatin proteins (HP1alpha, HP1beta, HP1gamma). However, the nontranscribed sequences were found predominantly at the nuclear periphery or at the nucleoli, whereas genes tended to localize on chromosome surfaces exposed to the nuclear interior. (C) 2004 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 15530862
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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: PEPTIDE ; EXPRESSION ; INVASION ; Germany ; human ; COHORT ; DISEASE ; DISEASES ; POPULATION ; RISK ; GENE ; GENOME ; HYBRIDIZATION ; PATIENT ; DNA ; INDUCTION ; colon ; polymorphism ; COMPARATIVE GENOMIC HYBRIDIZATION ; COPY NUMBER ; NUMBER ; HUMAN GENOME ; PEPTIDES ; POLYMERASE-CHAIN-REACTION ; INDIVIDUALS ; ULCERATIVE-COLITIS ; inflammation ; INFLAMMATORY-BOWEL-DISEASE ; CLUSTER ; DNA-SEQUENCE ; INTERVAL ; LOCUS ; chronic inflammation ; DEFICIENT ; SEGMENTAL DUPLICATIONS ; odds ratio ; genomic ; ALPHA-DEFENSIN ; DEFENSIN DEFICIENCY ; healthy individuals ; NOD2 ; PANETH CELLS ; RESIDENT INTESTINAL FLORA
    Abstract: Defensins are endogenous antimicrobial peptides that protect the intestinal mucosa against bacterial invasion. It has been suggested that deficient defensin expression may underlie the chronic inflammation of Crohn disease ( CD). The DNA copy number of the beta-defensin gene cluster on chromosome 8p23.1 is highly polymorphic within the healthy population, which suggests that the defective beta-defensin induction in colonic CD could be due to low beta-defensin gene copy number. Here, we tested this hypothesis, using genomewide DNA copy number profiling by array-based comparative genomic hybridization and quantitative polymerase-chain-reaction analysis of the human beta-defensin 2 (HBD-2) gene. We showed that healthy individuals, as well as patients with ulcerative colitis, have a median of 4 ( range 2 - 10) HBD-2 gene copies per genome. In a surgical cohort with ileal or colonic CD and in a second large cohort with inflammatory bowel diseases, those with ileal resections/disease exhibited a normal median HBD-2 copy number of 4, whereas those with colonic CD had a median of only 3 copies per genome ( for the surgical cohort; P = .008 P = .032 for the second cohort). Overall, the copy number distribution in colonic CD was shifted to lower numbers compared with controls ( for both the surgical cohort and the cohort with inflammatory bowel diseases). Individuals with P = .002 〈= 3 copies have a significantly higher risk of developing colonic CD than did individuals with 〉= 4 copies ( odds ratio 3.06; 95% confidence interval 1.46 - 6.45). An HBD-2 gene copy number of 〈 4 was associated with diminished mucosal HBD-2 mRNA expression (P = 0.033). In conclusion, a lower HBD-2 gene copy number in the beta-defensin locus predisposes to colonic CD, most likely through diminished beta-defensin expression
    Type of Publication: Journal article published
    PubMed ID: 16909382
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  • 6
    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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  • 7
    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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  • 8
    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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  • 9
    Keywords: EXPRESSION ; carcinoma ; CELL ; Germany ; human ; THERAPY ; GENE ; HYBRIDIZATION ; microarray ; PROTEIN ; TISSUE ; SURGERY ; ACTIVATION ; CONTRAST ; TARGET ; IN-SITU ; PROGRESSION ; AMPLIFICATION ; COMPARATIVE GENOMIC HYBRIDIZATION ; COPY NUMBER ; immunohistochemistry ; CATALYTIC SUBUNIT ; NUMBER ; metastases ; CANCER-CELLS ; HEAD ; CARCINOMAS ; NECK ; squamous cell carcinoma ; pathology ; FLUORESCENCE ; fluorescence in situ hybridization ; protein expression ; in situ hybridization ; CELL CARCINOMA ; development ; methods ; tissue microarray ; tissue microarray analysis ; CANDIDATE ; SQUAMOUS-CELL ; reverse transcriptase ; human telomerase ; IMMORTALITY ; oral squamous cell carcinoma ; TERT
    Abstract: BACKGROUND: Gene copy number gain of chromosomal arm 5p is frequently found in oral squamous cell carcinoma (OSCC) suggesting the activation of proto-oncogenes. TERT is a candidate gene encoding for human telomerase reverse transcriptase (hTERT). The aim of the present study was to elucidate the relevance of TERT copy number gain and high hTERT expression in OSCC. METHODS: Fluorescence in situ hybridization (FISH) for TERT and immunohistochemistry (IHC) for hTERT were performed to analyze TERT copy numbers and hTERT expression, respectively, on tissue microarray (TMA) sections including n = 247 OSCC and n = 105 pharyngeal and laryngeal squamous cell carcinomas (PSCC/LSCC). RESULTS: Increased hTERT protein expression was more frequently found in OSCC (71.1 %, 155/218) than in PSCC/LSCC (36.0%, 35/89) (13 〈 0.001). By contrast, specific TERT amplifications were less common in OSCC (2.1%, 4/191) compared with PSCC/LSCC (9.9%, 8/81) (P = 0.047). CONCLUSIONS: High hTERT expression is a frequent finding in OSCC. It might be a promising target for the development of specific anti-neoplastic therapy approaches
    Type of Publication: Journal article published
    PubMed ID: 17448136
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  • 10
    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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