Search results for "Chromosomal Instability"

showing 10 items of 15 documents

Spontaneous and Radiation-Induced Chromosome Aberrations in Primary Fibroblasts of Patients With Pediatric First and Second Neoplasms

2020

Frontiers in oncology 10, 1338 (2020). doi:10.3389/fonc.2020.01338

0301 basic medicineCancer ResearchDNA repairSomatic cell610Chromosomal translocationlcsh:RC254-28203 medical and health sciences0302 clinical medicineRadiation sensitivityChromosome instabilitymedicinechildhood cancerddc:610spontaneous chromosomal instabilityOriginal Researchmedicine.diagnostic_testbusiness.industryChromosomeradiation sensitivitysecond primary malignancieslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrimary Neoplasm030104 developmental biologychromosome aberrationsOncology030220 oncology & carcinogenesisCancer researchbusinessionizing radiationSecond primary malignancies ; Radiation sensitivity ; Chromosome aberrations ; Childhood cancer ; Spontaneous chromosomal instability ; Ionizing radiationFluorescence in situ hybridization
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NOTCH3 expression is linked to breast cancer seeding and distant metastasis

2018

Background Development of distant metastases involves a complex multistep biological process termed the invasion-metastasis cascade, which includes dissemination of cancer cells from the primary tumor to secondary organs. NOTCH developmental signaling plays a critical role in promoting epithelial-to-mesenchymal transition, tumor stemness, and metastasis. Although all four NOTCH receptors show oncogenic properties, the unique role of each of these receptors in the sequential stepwise events that typify the invasion-metastasis cascade remains elusive. Methods We have established metastatic xenografts expressing high endogenous levels of NOTCH3 using estrogen receptor alpha-positive (ERα+) MCF…

0301 basic medicineCancer ResearchTransplantation HeterologousNotch signaling pathwayEstrogen receptorMice NudeBreast NeoplasmsTriple Negative Breast NeoplasmsTumor stemneCentrosome amplificationTumor stemnessMetastasilcsh:RC254-282MetastasisMetastasis03 medical and health sciences0302 clinical medicineBreast cancerNeoplasm SeedingBreast cancerSurgical oncologyCell Line TumormedicineAnimalsHumansCell Self RenewalReceptor Notch3business.industryGene Expression ProfilingMiddle Agedmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrimary tumorSurvival Analysis3. Good healthChromosomal instabilityGene Expression Regulation NeoplasticSettore BIO/18 - Genetica030104 developmental biologyOncology030220 oncology & carcinogenesisCancer cellCancer researchMCF-7 CellsFemaleRNA InterferencebusinessBrain metastasisResearch ArticleBreast Cancer Research
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Induction of Chromosome Instability by Activation of Yes-Associated Protein and Forkhead Box M1 in Liver Cancer

2016

Background & Aims Many different types of cancer cells have chromosome instability. The hippo pathway leads to phosphorylation of the transcriptional activator yes-associated protein 1 (YAP1, YAP), which regulates proliferation and has been associated with the development of liver cancer. We investigated the effects of hippo signaling via YAP on chromosome stability and hepatocarcinogenesis in humans and mice. Methods We analyzed transcriptome data from 242 patients with hepatocellular carcinoma (HCC) to search for gene signatures associated with chromosomal instability (CIN); we investigated associations with overall survival time and cancer recurrence using Kaplan–Meier curves. We analyze…

0301 basic medicineTime FactorsMuscle ProteinsKaplan-Meier Estimatemedicine.disease_causeChromosome instabilityYAP1Liver NeoplasmsGastroenterologyTEA Domain Transcription FactorsHep G2 CellsPrognosisDNA-Binding ProteinsGene Expression Regulation NeoplasticPhenotypeHippo signalingRNA InterferenceSignal TransductionCarcinoma HepatocellularPorphyrinsAntineoplastic AgentsMice TransgenicBiologyTransfection03 medical and health sciencesChromosomal InstabilitymedicineAnimalsHumansGene silencingGenetic Predisposition to DiseaseAdaptor Proteins Signal TransducingHippo signaling pathwayHepatologyGene Expression ProfilingForkhead Box Protein M1VerteporfinYAP-Signaling ProteinsHCCSPhosphoproteinsThiostreptonMolecular biologyMice Inbred C57BLDisease Models Animal030104 developmental biologyTissue Array AnalysisFOXM1Cancer researchTranscriptomeCarcinogenesisTranscription FactorsGastroenterology
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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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Segmental duplication associated with evolutionary instability of human chromosome 3p25.1

2005

Fluorescence in situ hybridization (FISH) of human bacterial artificial chromosome (BAC) clones to orangutan metaphase spreads localized a breakpoint between human chromosome 3p25.1 and orangutan chromosome 2 to a <30-kb interval. The inversion occurred in a relatively gene-rich region with seven genes within 500 kb. The underlying breakpoint is closely juxtaposed to validated genes, however no functional gene has been disrupted by the evolutionary rearrangement. An approximately 21-kb DNA segment at the 3p25.1 breakpoint region has been duplicated intrachromosomally and interchromosomally to multiple regions in the orangutan and human genomes, providing additional evidence for the role …

BiologyEvolution MolecularChromosomal InstabilityGene DuplicationYeastsChromosome regionsGeneticsmedicineAnimalsHumansMolecular BiologyIn Situ Hybridization FluorescencePhylogenyGenetics (clinical)Segmental duplicationGeneticsBacterial artificial chromosomeGorilla gorillamedicine.diagnostic_testChromosome MappingKaryotypeChromosome 17 (human)KaryotypingChromosomes Human Pair 3Chromosome 21Chromosome 22Fluorescence in situ hybridizationCytogenetic and Genome Research
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Arsenic-induced DNA hypomethylation affects chromosomal instability in mammalian cells

2004

Early genetic instability induced in dividing V79-Cl3 Chinese hamster cells by inorganic arsenic, as demonstrated in our previous investigation, was evidenced by aneuploidy and nuclear abnormalities, but not by chromosomal rearrangements. Here we report the results of cytogenetic and morphological analyses performed on the progeny of cells dividing at the end of sodium arsenite treatment after they had been expanded through 120 generations (ASO cells) and then cloned. The acquired genetic instability persisted and was increased by highly unstable chromosomal rearrangements, namely dicentric chromosomes and telomeric associations, which were not seen following acute exposure. A peculiar find…

Cancer ResearchAneuploidyAntineoplastic Agentsgenomic instability arsenicChinese hamsterArsenicDicentric chromosomechemistry.chemical_compoundChromosome instabilityChromosomal InstabilityCricetinaemedicineAnimalsChromosome AberrationsbiologyChromosomeGeneral MedicineDNA Methylationmedicine.diseasebiology.organism_classificationMolecular biologySettore BIO/18 - GeneticachemistryDNA methylationCytogenetic AnalysisCarcinogensDNADNA hypomethylation
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Centrosome amplification induced by hydroxyurea leads to aneuploidy in pRB deficient human and mouse fibroblasts.

2006

Alterations in the number and/or morphology of centrosomes are frequently observed in human tumours. However, it is still debated if a direct link between supernumerary centrosomes and tumorigenesis exists and if centrosome amplification could directly cause aneuploidy. Here, we report that hydroxyurea treatment induced centrosome amplification in both human fibroblasts expressing the HPV16 -E6-E7 oncoproteins, which act principally by targeting p53 and pRB, respectively, and in conditional pRB deficient mouse fibroblasts. Following hydroxyurea removal both normal and p53 deficient human fibroblasts arrested. On the contrary pRB deficient fibroblasts entered the cell cycle generating aneupl…

Cancer ResearchAneuploidyCentrosome amplificationBiologymedicine.disease_causeRetinoblastoma ProteinCell LineMicepRBChromosomal InstabilitymedicineDeficient mouseAnimalsHumansHydroxyureaCINCells CulturedCentrosomeDNA synthesisCell cycleFibroblastsmedicine.diseaseAneuploidyCell biologySettore BIO/18 - GeneticaOncologyCentrosomeAneuploid CellsCarcinogenesisCancer letters
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Metabolic aggressiveness in benign meningiomas with chromosomal instabilities.

2010

Abstract Meningiomas are often considered benign tumors curable by surgery, but most recurrent meningiomas correspond to histologic benign tumors. Because alterations in chromosome 14 among others have suggested clinical aggressiveness and recurrence, determining both the molecular phenotype and the genetic profile may help distinguish tumors with aggressive metabolism. The aim of this study was to achieve higher specificity in the detection of meningioma subgroups by measuring chromosomal instabilities by fluorescence in situ hybridization and cytogenetics and metabolic phenotypes by high-resolution magic angle spinning spectroscopy. We studied 46 meningioma biopsies with these methodologi…

Cancer Researchmedicine.medical_specialtyPathologyMagnetic Resonance SpectroscopyBiologyMeningiomaChromosomal Instabilityotorhinolaryngologic diseasesmedicineMeningeal NeoplasmsTumor Cells CulturedHumansIn Situ Hybridization FluorescenceNeoplasm StagingChromosome Aberrationsmedicine.diagnostic_testCytogeneticsCancerChromosomemedicine.diseasePhenotypenervous system diseasesOncologyApoptosisBenign MeningiomaCytogenetic AnalysisMetabolomeMeningiomaFluorescence in situ hybridizationCancer research
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Simultaneous Aurora-A/STK15 overexpression and centrosome amplification induce chromosomal instability in tumour cells with a MIN phenotype

2007

Abstract Background Genetic instability is a hallmark of tumours and preneoplastic lesions. The predominant form of genome instability in human cancer is chromosome instability (CIN). CIN is characterized by chromosomal aberrations, gains or losses of whole chromosomes (aneuploidy), and it is often associated with centrosome amplification. Centrosomes control cell division by forming a bipolar mitotic spindle and play an essential role in the maintenance of chromosomal stability. However, whether centrosome amplification could directly cause aneuploidy is not fully established. Also, alterations in genes required for mitotic progression could be involved in CIN. A major candidate is represe…

Genome instabilityCancer ResearchCellular differentiationAneuploidyApoptosisCell CommunicationSpindle ApparatusBiologyProtein Serine-Threonine Kinaseslcsh:RC254-282Aurora KinasesChromosome instabilityChromosomal InstabilitymedicineTumor Cells CulturedGeneticsHumansRNA Small InterferingMitosisIn Situ Hybridization FluorescenceAurora Kinase ACentrosomePloidiesReverse Transcriptase Polymerase Chain ReactionAurora-A centrosomes amplification aneuploidyCell Differentiationlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseAneuploidyCell biologySpindle apparatusUp-RegulationSettore BIO/18 - GeneticaCell Transformation NeoplasticPhenotypeMicroscopy FluorescenceOncologyCentrosomeColonic NeoplasmsEctopic expressionMicrosatellite InstabilityResearch ArticleBMC Cancer
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MAD2 depletion triggers premature cellular senescence in human primary fibroblasts by activating a P53 pathway preventing aneuploid cells propagation.

2012

The spindle assembly checkpoint (SAC) is a cellular surveillance mechanism that ensures faithful chromosome segregation during mitosis and its failure can result in aneuploidy. Previously, it was suggested that reduction of the MAD2 gene, encoding a major component of the SAC, induced aneuploidy in human tumor cells. However, tumor cell lines contain multiple mutations that might affect or exacerbate the cellular response to Mad2 depletion. Thus, the scenario resulting by Mad2 depletion in primary human cells could be different and more complex that the one depicted so far. We used primary human fibroblasts (IMR90) and epithelial breast cells (MCF10A) to gain further insight on the effects …

Genome instabilityCyclin-Dependent Kinase Inhibitor p21Cell cycle checkpointMad2PhysiologyClinical BiochemistryMAD2 depletion Aneuploidy Premature cellular senescence TP53Cell Cycle ProteinsBiologyCyclin-dependent kinaseChromosome instabilityChromosomal InstabilityTumor Suppressor Protein p14ARFHumansGene SilencingRNA Small InterferingMitosisCells CulturedCellular SenescenceCell ProliferationCalcium-Binding ProteinsCell BiologyCell Cycle CheckpointsFibroblastsAneuploidybeta-GalactosidaseCell biologyRepressor ProteinsSpindle checkpointSettore BIO/18 - GeneticaGene Expression RegulationMad2 Proteinsbiology.proteinM Phase Cell Cycle CheckpointsTumor Suppressor Protein p53Cell agingSignal Transduction
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