Search results for "aneuploidy"

showing 10 items of 113 documents

MYC dosage compensation is mediated by miRNA-transcription factor interactions in aneuploid cancer

2021

Summary We hypothesize that dosage compensation of critical genes arises from systems-level properties for cancer cells to withstand the negative effects of aneuploidy. We identified several candidate genes in cancer multiomics data and developed a biocomputational platform to construct a mathematical model of their interaction network with micro-RNAs and transcription factors, where the property of dosage compensation emerged for MYC and was dependent on the kinetic parameters of its feedback interactions with three micro-RNAs. These circuits were experimentally validated using a genetic tug-of-war technique to overexpress an exogenous MYC, leading to overexpression of the three microRNAs …

Candidate geneMultidisciplinaryDosage compensationColorectal cancerBioinformaticsScienceQCancerMycBiologymedicine.diseaseArticleDownregulation and upregulationCancer cellmicroRNATranscription factorsmedicineCancer researchcancerDosage compensationaneuploidyMathematical biosciencesSystems biologyTranscription factormiRNAiScience
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Simultaneous reduction of MAD2 and BUBR1 expression induces mitotic spindle alterations associated with p53 dependent cell cycle arrest and death

2014

Most human tumors are characterized by aneuploidy that is believed to be the consequence of chromosomal instability (CIN). The mechanism(s) leading to aneuploidy and the pathways that allow its tolerance are not completely understood. The Spindle Assembly Checkpoint (SAC) is a cellular surveillance mechanism working during mitosis, and alterations of genes that encode components of the SAC weakening the mitotic checkpoint, induce aneuploidy by chromosome mis-segregation. We induced aneuploidy in near-diploid tumor cells by simultaneous depletion of the SAC proteins MAD2 and BUBR1 by RNA interference in the attempt to gain further insight on the cellular responses to aneuploidy. Individual r…

Cell cycle checkpointMad2AneuploidyCell BiologyGeneral MedicineCell cycleBiologymedicine.diseaseSpindle apparatusCell biologySpindle checkpointChromosome instabilitymedicineMitosisCell Biology International
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Clastogenic and aneuploidizing effects of antiblastic busulphan revealed by kinetochore immunofluorescence in CHO cells.

1991

We utilized, in CHO cells, the cytoplasm preservation technique to evaluate the micronucleus frequency at different busulphan concentrations, and the indirect immunofluorescence technique, using sera obtained from patients with scleroderma (CREST variant), to analyze if busulphan-induced micronuclei have kinetochores. Results show that this alkylating agent is capable of causing a significant increase of micronuclei in vitro, a great part (40%) of them having CREST-positive kinetochores. These findings confirm the clastogenic effect of busulphan and reveal a considerable capability of this agent to induce aneuploidy. These results are examined taking into account the high incidence of secon…

CentromereAneuploidyFluorescent Antibody TechniqueBiologyImmunofluorescenceCell LineAcetoneClastogenhemic and lymphatic diseasesmedicineHumansBusulfanMicronuclei Chromosome-DefectiveChromosome AberrationsMicronucleus TestsScleroderma Systemicmedicine.diagnostic_testDose-Response Relationship DrugGeneral Medicinemedicine.diseaseAneuploidyMolecular biologyIn vitroCell cultureMicronucleus testMicronucleusBusulfanmedicine.drugMutation research
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Congenital hypopituitarism and multiple midline defects in a newborn with non-familial Cat Eye syndrome

2022

Abstract Background Cat eye syndrome (CES) is a rare chromosomal disease, with estimated incidence of about 1 in 100,000 live newborns. The classic triad of iris coloboma, anorectal malformations, and auricular abnormalities is present in 40% of patients, and other congenital defects may also be observed. The typical associated cytogenetic anomaly relies on an extra chromosome, derived from an inverted duplication of short arm and proximal long arm of chromosome 22, resulting in partial trisomy or tetrasomy of such regions (inv dup 22pter-22q11.2). Case presentation We report on a full-term newborn, referred to us soon after birth. Physical examination showed facial dysmorphisms, including …

Chromosome Aberrations...CholestasisHydrocortisoneCongenital hypopituitarismSupernumerary marker chromosomeChromosomes Human Pair 22Chromosome DisordersGeneral MedicineCESAneuploidyChromosome AberrationHypoglycemiaHypopituitarismColobomaEye AbnormalitieChromosome DisorderCholestasiCase reportHumansFemaleEye AbnormalitiesNeonatal hypoglycemiaItalian Journal of Pediatrics
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Aneuploid IMR90 cells induced by depletion of pRB, DNMT1 and MAD2 show a common gene expression signature

2019

Chromosome segregation defects lead to aneuploidy which is a major feature of solid tumors. How diploid cells face chromosome mis-segregation and how aneuploidy is tolerated in tumor cells are not completely defined yet. Thus, an important goal of cancer genetics is to identify gene networks that underlie aneuploidy and are involved in its tolerance. To this aim, we induced aneuploidy in IMR90 human primary cells by depleting pRB, DNMT1 and MAD2 and analyzed their gene expression profiles by microarray analysis. Bioinformatic analysis revealed a common gene expression profile of IMR90 cells that became aneuploid. Gene Set Enrichment Analysis (GSEA) also revealed gene-sets/pathways that are …

DNA (Cytosine-5-)-Methyltransferase 1AneuploidyBiologyMicroarrayReal-Time Polymerase Chain ReactionRetinoblastoma ProteinCell LineRNA interferenceGene expressionProtein Interaction MappingGeneticsmedicineHumansGeneOligonucleotide Array Sequence AnalysisMicroarray analysis techniquesGene Expression ProfilingBioinformatics analysiChromosomeFibroblastsmedicine.diseaseAneuploidyGene Expression RegulationRNAiMad2 ProteinsDNMT1Cancer researchKIF4ARNA InterferenceTranscriptomeIMR90 human fibroblast
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DNA integrity, growth pattern, spindle formation, chromosomal constitution and imprinting patterns of mouse oocytes from vitrified pre-antral follicl…

2010

Cryopreservation of follicles for culture and oocyte growth and maturation in vitro provides an option to increase the number of fertilizable oocytes and restore fertility in cases where transplantation of ovarian tissue poses a risk for malignant cell contamination. Vitrification for cryopreservation is fast and avoids ice crystal formation. However, the influences of exposure to high concentrations of cryoprotectants on follicle development, oocyte growth and maturation, and particularly, on the DNA integrity and methylation imprinting has not been studied systematically. Follicle survival and development, DNA damage, oocyte growth patterns, maturation, spindle formation and chromosomal c…

DNA RepairSpindle ApparatusBiologyCryopreservationsnRNP Core ProteinsAndrologyGenomic ImprintingMiceOogenesisOvarian FolliclemedicineAnimalsaneuploidyOvarian follicleGeneticsCryopreservationRehabilitationObstetrics and GynecologyDNADNA MethylationAntral follicleOocyteVitrificationTransplantationMice Inbred C57BLmedicine.anatomical_structureDifferentially methylated regionsoocyte maturationReproductive MedicineDNA methylationMice Inbred CBAOocytesDNA damageCpG IslandsFemaleimprintingGenomic imprintingcryopreseration
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Functional Inactivation of pRB Results in Aneuploid Mammalian Cells After Release From a Mitotic Block

2002

AbstractThe widespread chromosome instability observed in tumors and in early stage carcinomas suggests that aneuploidy could be a prerequisite for cellular transformation and tumor initiation. Defects in tumor suppressers and genes that are part of mitotic checkpoints are likely candidates for the aneuploid phenotype. By using flow cytometric, cytogenetic, immunocytochemistry techniques we investigated whether pRB deficiency could drive perpetual aneuploidy in normal human and mouse fibroblasts after mitotic checkpoint challenge by microtubule-destabilizing drugs. Both mouse and human pRB-deficient primary fibroblasts resulted, upon release from a mitotic block, in proliferating aneuploid …

DNA ReplicationCancer ResearchBrief ArticleClone (cell biology)MitosisAneuploidyCre recombinaseSpindle Apparatuslcsh:RC254-282Retinoblastoma ProteinColony-Forming Units AssayMicechemistry.chemical_compoundChromosome instabilitymedicineAnimalsHumanscentrosomesCINGenes RetinoblastomaMitosisCells CulturedIn Situ Hybridization FluorescenceCentrosomeCell cycle controlbiologyColcemidChromosome FragilityCell CycleGINDemecolcineRetinoblastoma proteinAneuploidy; Cell cycle control; Centrosomes; CIN; PRB;FibroblastsCell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensAneuploidyFlow Cytometrymedicine.diseaseAntineoplastic Agents PhytogenicCell biologyCell Transformation NeoplasticPRBMicroscopy Fluorescencechemistrybiology.proteinFemaleNeoplasia
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Cisplatin-induced endoreduplication in CHO cells: DNA damage and inhibition of topoisomerase II.

2006

It has been proposed that polyploid cells that arise during a variety of pathological conditions and as a result of exposure to genotoxicants, typically in the liver, become aneuploid through genetic instability. Aneuploidy contributes to, or even drives, tumour development. We have assessed the capacity of the drug cisplatin, one of the most commonly used compounds for the treatment of malignancies, to induce endoreduplication, a particular type of polyploidy, in cultured Chinese hamster AA8 cells. Taking into account that any interference with DNA topoisomerase II (topo II) function leads to endoreduplication, we have found that treatment of the cells with this platinum compound results i…

DNA damageHealth Toxicology and MutagenesisAntineoplastic AgentsCHO CellsPolyploidychemistry.chemical_compoundCricetinaeGeneticsmedicineEndoreduplicationAnimalsHumansTopoisomerase II InhibitorsEnzyme InhibitorsMolecular BiologyCisplatinbiologySettore BIO/16 - Anatomia UmanaTopoisomeraseChinese hamster ovary cellNeoplasms Second PrimaryCell cycleAneugensAneuploidyMolecular biologychemistryTopoisomerase II cisplatinbiology.proteinCancer researchTopoisomerase-II InhibitorCisplatinDNAmedicine.drugDNA Damage
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Checkpoint adaptation in repair-deficient cells drives aneuploidy and resistance to genotoxic agents

2018

AbstractHuman cancers frequently harbour mutations in DNA repair genes, rendering the use of DNA damaging agents as an effective therapeutic intervention. As therapy-resistant cells often arise, it is important to better understand the molecular pathways that drive resistance in order to facilitate the eventual targeting of such processes. We employ repair-defective diploid yeast as a model to demonstrate that, in response to genotoxic challenges, nearly all cells eventually undergo checkpoint adaptation, resulting in the generation of aneuploid cells with whole chromosome losses that have acquired resistance to the initial genotoxic challenge. We demonstrate that adaptation inhibition, eit…

DNA repairAneuploidyBiologymedicine.diseasePhenotypeYeastCell biologychemistry.chemical_compoundchemistrymedicinePloidyAdaptationCytotoxicityDNA
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“DNA Methyl transferase 1 post-trascriptional silencing indues aneuploidy and cell cycle arrest in human cells”,

2009

DNMT1 aneuploidy
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