Search results for "Chromosome Fragility"

showing 4 items of 4 documents

FANCD2 modulates the mitochondrial stress response to prevent common fragile site instability

2021

Common fragile sites (CFSs) are genomic regions frequently involved in cancer-associated rearrangements. Most CFSs lie within large genes, and their instability involves transcription- and replication-dependent mechanisms. Here, we uncover a role for the mitochondrial stress response pathway in the regulation of CFS stability in human cells. We show that FANCD2, a master regulator of CFS stability, dampens the activation of the mitochondrial stress response and prevents mitochondrial dysfunction. Genetic or pharmacological activation of mitochondrial stress signaling induces CFS gene expression and concomitant relocalization to CFSs of FANCD2. FANCD2 attenuates CFS gene transcription and pr…

0301 basic medicineGenome instabilitymusculoskeletal diseasesTranscription GeneticQH301-705.5RegulatorMedicine (miscellaneous)MitochondrionBiology[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGeneral Biochemistry Genetics and Molecular BiologyOxidative PhosphorylationArticle03 medical and health sciences0302 clinical medicineTranscription (biology)Stress Physiologicalhemic and lymphatic diseasesGene expressionFANCD2HumansBiology (General)GeneUbiquitinsChromosomal fragile siteChromosome Fragile SitesChromosome FragilityFanconi Anemia Complementation Group D2 ProteinDNA damage and repair[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyHCT116 CellsCell biologyMitochondriaSettore BIO/18 - Genetica030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisUnfolded Protein ResponseGeneral Agricultural and Biological SciencesDNA Damage
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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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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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Family studies in scleroderma (systemic sclerosis) demonstrating an HLA-linked increased chromosomal breakage rate in cultured lymphocytes

1988

An increased chromosomal breakage rate (ICBR) was found in 27 of 28 patients with scleroderma (systemic sclerosis, SS) - 5 with the syndrome including calcinosis cutis, Raynaud phenomenon, esophagus hypomotility, sclerodactyly and telangiectasia (CREST), 4 incomplete CREST, 1 overlapping syndrome, 18 progressive systemic sclerosis (PSS). Not only the patients, but also about half of their first-degree relatives showed an increased chromosomal breakage rate (more than 5 breaks per 100 metaphases). This character segregated as a dominant marker in nine families of scleroderma patients. In the six informative of the nine families, the ICBR trait showed close linkage with the HLA region on chro…

Genetic MarkersMaleSystemic diseaseGenetic LinkageHuman leukocyte antigenBiologySclerodermaCalcinosis cutisHLA AntigensGeneticsmedicineHumansLymphocytesCells CulturedGenetics (clinical)Chromosome AberrationsAutoimmune diseaseScleroderma SystemicSclerodactylyChromosome Fragilitymedicine.diseaseConnective tissue diseasePedigreeHaplotypesImmunologyFemalemedicine.symptomHuman Genetics
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