Search results for "Gene Amplification"

showing 10 items of 100 documents

New pattern of EGFR amplification in glioblastoma and the relationship of gene copy number with gene expression profile

2010

Gene amplification is a process that is characterized by an increase in the copy number of a restricted region in a chromosome arm, and is frequently associated with an overexpression of the corresponding amplified gene. Amplified DNA can be organized either as extrachromosomal elements, repeated units at a single locus or scattered throughout the genome. The amplification of the gene for epidermal growth factor receptor (EGFR) is a common finding in glioblastomas and the amplified gene copies appears as double minutes. The aim of this study was to investigate the different patterns of EGFR amplification in 40 cases of glioblastoma using FISH analysis in metaphases and paraffin sections, an…

AdultMaleGene DosageBiologyPolymerase Chain ReactionPolymorphism Single NucleotideGene dosagePathology and Forensic MedicineYoung AdultGene expressionGene duplicationTumor Cells CulturedHumansDouble minuteRNA MessengerCopy-number variationGeneIn Situ Hybridization FluorescenceAgedOligonucleotide Array Sequence AnalysisChromosome 7 (human)Regulation of gene expressionBrain NeoplasmsGene Expression ProfilingGene AmplificationMiddle AgedImmunohistochemistryMolecular biologyErbB ReceptorsGene Expression Regulation NeoplasticMutagenesis InsertionalFemaleGlioblastomaChromosomes Human Pair 7Modern Pathology
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Alternative lengthening of telomeres--an enhanced chromosomal instability in aggressive non-MYCN amplified and telomere elongated neuroblastomas

2010

Telomere length alterations are known to cause genomic instability and influence clinical course in several tumor types, but have been little investigated in neuroblastoma (NB), one of the most common childhood tumors. In the present study, telomere-dependent chromosomal instability and telomere length were determined in six NB cell lines and fifty tumor biopsies. The alternative lengthening of telomeres (ALT) pathway was assayed by scoring ALT-associated promyelocytic leukemia (PML) bodies (APBs). We found a reduced probability of overall survival for tumors with increased telomere length compared to cases with reduced or unchanged telomere length. In non-MYCN amplified tumors, a reduced o…

AdultMaleGenome instabilityCancer ResearchBiologyNeuroblastomaYoung AdultCell Line TumorChromosomal InstabilityChromosome instabilityNeuroblastomaGeneticsmedicineHumansChildTelomeraseIn Situ Hybridization FluorescenceAnaphaseOncogene ProteinsN-Myc Proto-Oncogene ProteinOncogeneGene AmplificationInfant NewbornInfantNuclear ProteinsTelomeremedicine.diseaseMolecular biologyTelomereLeukemiaCell cultureChild PreschoolFemaleAnaphase
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Safety and Activity of the First-in-Class Sym004 Anti-EGFR Antibody Mixture in Patients with Refractory Colorectal Cancer

2015

Abstract Tumor growth in the context of EGFR inhibitor resistance may remain EGFR-dependent and is mediated by mechanisms including compensatory ligand upregulation and de novo gene alterations. Sym004 is a two-antibody mixture targeting nonoverlapping EGFR epitopes. In preclinical models, Sym004 causes significant EGFR internalization and degradation, which translates into superior growth inhibition in the presence of ligands. In this phase I trial, we observed grade 3 skin toxicity and hypomagnesemia as mechanism-based dose-limiting events during dose escalation. In dose-expansion cohorts of 9 and 12 mg/kg of Sym004 weekly, patients with metastatic colorectal cancer and acquired EGFR inhi…

AdultMaleProto-Oncogene Proteins B-rafClass I Phosphatidylinositol 3-KinasesColorectal cancerCancer development and immune defence Radboud Institute for Molecular Life Sciences [Radboudumc 2]Antineoplastic AgentsContext (language use)Rare cancers Radboud Institute for Molecular Life Sciences [Radboudumc 9]LigandsPhosphatidylinositol 3-Kinaseschemistry.chemical_compoundCell Line TumorHumansMedicinePanitumumabNeoplasm MetastasisAgedEGFR inhibitorsAged 80 and overDose-Response Relationship DrugCetuximabbusiness.industryGene AmplificationAntibodies MonoclonalCancerMiddle Agedmedicine.diseaseErbB ReceptorsClinical trialGenes rasTreatment OutcomeOncologychemistryMutationImmunologyCancer researchFemaleGrowth inhibitionColorectal Neoplasmsbusinessmedicine.drug
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Phenotype Correlation and Intergenerational Dynamics of the Friedreich Ataxia GAA Trinucleotide Repeat

1997

Summary The Friedreich ataxia (FA) mutation has recently been identified as an unstable trinucleotide GAA repeat present 7–22 times in the normal population but amplified as many as > 1, 000 times in FA. Since it is an autosomal recessive disease, FA does not show typical features observed in other dynamic mutation disorders, such as genetic anticipation. We have analyzed the GAA repeat in 104 FA patients and 163 carrier relatives previously defined by linkage analysis. The GAA expansion was detected in all patients, most (94%) of them being ho-mozygous for the mutation. We have demonstrated that clinical variability in FA is related to the size of the expanded alleles: milder forms of the …

AtaxiaAdolescentGenetic LinkagePopulationBiologyTrinucleotide RepeatsMeiosisGenetic linkageGene duplicationGeneticsmedicineHumansGenetics(clinical)AlleleChildeducationGenetics (clinical)Geneticseducation.field_of_studyGene AmplificationPhenotypeFriedreich AtaxiaMutationMutation (genetic algorithm)Dynamic mutationmedicine.symptomResearch ArticleThe American Journal of Human Genetics
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Usefulness of omp1 restriction mapping for avian Chlamydia psittaci isolate differentiation

1995

Abstract Sixty-five avian Chlamydia psittaci isolates collected worldwide, including 27 previously characterized reference strains, were analysed by restriction mapping of the major outer membrane protein gene ( omp1 ) obtained after DMA amplification by PCR. They were compared to 2 ruminant isolates, a feline pneumonitis and a guinea pig inclusion conjunctivitis (GPIC) isolate. According to their omp1 restriction patterns, avian strains were heterogeneous in that they exhibited 6 and 4 distinct patterns using Alu I and Mbo II restriction enzymes, respectively, thus defining 7 groups. However, 84% of the studied strains belonged to groups 1 to 4, which share a specific fragment triplet of 4…

Base pairGuinea PigsRestriction MappingAMPLIFICATION CHAINE POLYMERASEIn Vitro TechniquesMicrobiologyBirdsRestriction mapAnimalsMolecular BiologyGene[SDV.MP] Life Sciences [q-bio]/Microbiology and ParasitologyElectrophoresis Agar GelChlamydia psittaciGeneticsbiologyDNA–DNA hybridizationGene AmplificationGeneral Medicinebiology.organism_classificationRestriction enzyme[SDV.MP]Life Sciences [q-bio]/Microbiology and ParasitologyChlamydophila psittaciGenes BacterialGenetic markerCatsCattleRestriction fragment length polymorphismBacterial Outer Membrane Proteins
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MYCN gain and MYCN amplification in a stage 4S neuroblastoma.

2003

Abstract Stage 4S neuroblastoma is a disease associated with spontaneous regression and good survival. We present a patient whose evolution has shown the variety and complexity of this disease in infants. Biologic factors, such as ploidy, MYCN copy number, loss of 1p36, and other chromosomal gains and losses were determined. A complex pattern of genetic abnormalities, such as near-diploidy, MYCN gain (2–4 copies per haploid genome) and imbalance/deletion of 1p36 was seen in the diagnostic sample. An extensive disseminated disease after a latent period of 26 months was associated with a special genetic evolution, such as tetraploidy, MYCN amplification (2:100–500 copies), 1p36 deletion, and …

Cancer ResearchAdrenal Gland NeoplasmsGenes mycDiseaseBiologymedicine.disease_causeNeuroblastomaFatal OutcomeNeuroblastomaGene duplicationGeneticsmedicineHumansneoplasmsMolecular BiologyNeoplasm StagingGeneticsMutationTransition (genetics)Gene AmplificationInfantmedicine.diseaseAneuploidyPrimary tumorChromosomes Human Pair 1Stage 4S NeuroblastomaCancer researchDisease ProgressionFemalePloidyChromosome DeletionChromosomes Human Pair 17Cancer genetics and cytogenetics
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Expression of type I interferon receptor and its relation with other prognostic factors in human neuroblastoma.

1998

Expression of type I interferon receptor (IFN-R) has been found in several normal tissues and in malignant neoplasms, mainly those with epithelial differentiation. In order to analyze the immunohistochemical expression of type I IFN-R we studied 79 cases of neuroblastoma. Results of expression of type I IFN-R were statistically correlated with histopathology, stage, bcl-2 and PCNA expression, N-myc amplification and apoptosis. We found expression of type I IFN-R in 54/79 cases showing statistical correlation with bcl-2 expression (P=0.017) and favourable histopathology (P=0.015). The overexpression found in ganglion cells suggests that IFN-R could be involved in the pathway of neuroblastoma…

Cancer ResearchCellular differentiationmedicine.medical_treatmentGenes mycAlpha interferonApoptosisReceptor Interferon alpha-betaBiologyImmunoenzyme TechniquesNeuroblastomaProliferating Cell Nuclear AntigenNeuroblastomaGene expressionBiomarkers TumormedicineHumansChildInterferon alfaNeoplasm StagingReceptors InterferonOncogeneGene AmplificationInfantMembrane ProteinsCell DifferentiationGeneral MedicinePrognosismedicine.diseaseNeoplasm ProteinsCytokineProto-Oncogene Proteins c-bcl-2OncologySpainChild PreschoolCancer researchImmunohistochemistrymedicine.drugOncology Reports
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Acquired resistance of melanoma cells to the antineoplastic agent fotemustine is caused by reactivation of the DNA repair gene mgmt

2001

Acquired resistance to antineoplastic agents is a frequent obstacle in tumor therapy. Malignant melanoma cells are particularly well known for their unresponsiveness to chemotherapy; only about 30% of tumors exhibit a transient clinical response to treatment. In our study, we investigated the molecular mechanism of acquired resistance of melanoma cells (MeWo) to the chloroethylating drug fotemustine. Determination of O6-methylguanine-DNA methyltransferase (MGMT) activity showed that MeWo cells that acquired resistance to fotemustine upon repeated treatment with the drug display high MGMT activity, whereas the parental cell line had no detectable MGMT. The resistant cell lines exhibit cross-…

Cancer ResearchGuanineMethyltransferaseDNA RepairDNA repairmedicine.medical_treatmentGene ExpressionAntineoplastic AgentsDrug resistanceBiologyNitrosourea CompoundsO(6)-Methylguanine-DNA MethyltransferaseEnzyme ReactivatorsOrganophosphorus CompoundsTumor Cells CulturedmedicineHumansEnzyme InhibitorsPromoter Regions GeneticMelanomaneoplasmsChemotherapyMelanomaGene AmplificationDNA Methylationmedicine.diseaseVirologydigestive system diseasesEnzyme ActivationBlotting SouthernOncologyDrug Resistance NeoplasmDNA methylationAzacitidineCancer researchFotemustinemedicine.drugAlkyltransferaseInternational Journal of Cancer
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Chimeric amplicons containing the c-myc gene in HL60 cells

1998

The major amplicon present in HL60 cells is chimeric in nature being composed of 70 kb of DNA sequence derived from the MYC locus linked to 80 kb of novel DNA sequence derived from a non contiguous region located telomeric to the c-myc gene at 8q24 (Feo et al., 1996). Here we show by fluorescence in situ hybridization (FISH) that these coamplified sequences, MCR (Myc Coamplified Region), are derived from a locus located 3-4 Mb telomeric to the c-myc gene in the q24.2-24.3 region of chromosome 8. Genomic cloning and Southern blot analysis indicate the arrangement of chimeric amplicons are in tandem arrays. Analysis of the DNA sequences at the juncture of the MYC locus and the MCR suggest tha…

Cancer ResearchOncogene Proteins FusionInverted repeatMolecular Sequence DataGenes mycHL-60 CellsLocus (genetics)BiologyMolecular cloningDNA sequencingLeukemia Promyelocytic AcuteGene mappingGeneticsHumansCloning MolecularMolecular BiologyGeneIn Situ Hybridization FluorescenceSouthern blotChromosome AberrationsRecombination GeneticGeneticsBase SequenceChromosome FragilityGene AmplificationSequence Analysis DNAAmpliconMolecular biologyBlotting SouthernChromosomes Human Pair 8Oncogene
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RB acute loss induces centrosome amplification and aneuploidy in murine primary fibroblasts

2006

AbstractBackgroundIncorrect segregation of whole chromosomes or parts of chromosome leads to aneuploidy commonly observed in cancer. The correct centrosome duplication, assuring assembly of a bipolar mitotic spindle, is essential for chromosome segregation fidelity and preventing aneuploidy. Alteration of p53 and pRb functions by expression of HPV16-E6 and E7 oncoproteins has been associated with centrosome amplification. However, these last findings could be the result of targeting cellular proteins in addition to pRb by HPV16-E7 oncoprotein. To get a more detailed picture on the role of pRb in chromosomal instability and centrosome amplification, we analyzed the effects of the acute loss …

Cancer ResearchTime FactorsTranscription GeneticRbCentrosomes AneuploidyGene ExpressionMitosisAneuploidyBiologyRetinoblastoma Proteinlcsh:RC254-282Chromosome segregationMiceChromosome instabilityGene duplicationmedicineAnimalsCentrosome duplicationMitosisCells CulturedCentrosomeResearchGene AmplificationFibroblastsAneuploidylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseSettore BIO/18 - GeneticaSpindle checkpointOncologyCentrosomeCancer researchMolecular MedicineMolecular Cancer
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