Search results for "Blastoma"

showing 10 items of 603 documents

A New Mutation of the p53 Gene in Human Neuroblastoma, Not Correlated with N-myc Amplification

1999

N-myc gene amplification and/or loss of heterozygosity of chromosome 1 (LOH lp) are important criteria for prognosis and progression in human neuroblastoma (NB). Despite the high incidence of alterations of the p53 gene in human cancers, very few p53 mutations have been reported in NB. The objective of our study was to search for p53 mutations in NB and their correlation with N-myc amplification and clinical or pathologic parameters. We analyzed 14 selected cases of NB from the Spanish Protocol N-II-92. We found a missense mutation in codon 248 CGG to GGG (Arg/Gly) in one case of stage 4 NB with no N-myc amplification. Our results confirm the low incidence of p53 gene mutation in neuroblas…

0301 basic medicineChromosomeBiologyGene mutationmedicine.diseaseMolecular biologyPathology and Forensic MedicineLoss of heterozygosity03 medical and health sciences030104 developmental biology0302 clinical medicine030220 oncology & carcinogenesisNeuroblastomaGene duplicationmedicineCancer researchMissense mutationSurgeryAnatomyGeneN-MycInternational Journal of Surgical Pathology
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Cyclins B1, T1, and H differ in their molecular mode of interaction with cytomegalovirus protein kinase pUL97

2019

Human cytomegalovirus (HCMV) is a common β-herpesvirus causing life-long latent infections. HCMV replication interferes with cell cycle regulation in host cells because the HCMV-encoded cyclin-dependent kinase (CDK) ortholog pUL97 extensively phosphorylates the checkpoint regulator retinoblastoma protein. pUL97 also interacts with cyclins B1, T1, and H, and recent findings have strongly suggested that these interactions influence pUL97 substrate recognition. Interestingly, here we detected profound mechanistic differences among these pUL97-cyclin interactions. Our study revealed the following. (i) pUL97 interacts with cyclins B1 and H in a manner dependent on pUL97 activity and HCMV-specifi…

0301 basic medicineCyclin H[SDV]Life Sciences [q-bio]CytomegalovirusVirus ReplicationBiochemistry03 medical and health sciencesCyclin HViral ProteinsProtein DomainsCyclin-dependent kinaseHumansProtein phosphorylationCyclin B1PhosphorylationCyclin B1Protein Structure QuaternaryMolecular BiologyComputingMilieux_MISCELLANEOUSCyclin030102 biochemistry & molecular biologybiologyChemistryCyclin TRetinoblastoma proteinCell BiologyCell cycle3. Good healthCell biology030104 developmental biologyHEK293 Cellsbiology.proteinCyclin-dependent kinase 7
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The MRN complex is transcriptionally regulated by MYCN during neural cell proliferation to control replication stress

2015

The MRE11/RAD50/NBS1 (MRN) complex is a major sensor of DNA double strand breaks, whose role in controlling faithful DNA replication and preventing replication stress is also emerging. Inactivation of the MRN complex invariably leads to developmental and/or degenerative neuronal defects, the pathogenesis of which still remains poorly understood. In particular, NBS1 gene mutations are associated with microcephaly and strongly impaired cerebellar development, both in humans and in the mouse model. These phenotypes strikingly overlap those induced by inactivation of MYCN, an essential promoter of the expansion of neuronal stem and progenitor cells, suggesting that MYCN and the MRN complex migh…

0301 basic medicineDNA ReplicationTranscription GeneticDNA damageDNA repairDNA-Binding ProteinCell Cycle ProteinsBiology03 medical and health sciencesMRE11 Homologue ProteinCell Cycle ProteinStrand-Break Repair; N-Myc; Dna-Replication; Human Neuroblastoma; Feingold-Syndrome; C-Myc; Mre11-Rad50-Nbs1 Complex; Targeted Disruption; Genomic Instability; Embryonic LethalityHumansProgenitor cellMolecular BiologyneoplasmsCells CulturedNuclear ProteinCell ProliferationGeneticsNeuronsOncogene ProteinsOriginal PaperMRE11 Homologue ProteinN-Myc Proto-Oncogene ProteinCell growthDNA Repair EnzymeDNA replicationOncogene ProteinNuclear ProteinsCell BiologyNeuronCell biologyAcid Anhydride HydrolasesDNA-Binding Proteins030104 developmental biologyDNA Repair EnzymesMRN complexGene Expression RegulationRad50HumanCell Death and Differentiation
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Identification of novel drug resistance mechanisms by genomic and transcriptomic profiling of glioblastoma cells with mutation-activated EGFR.

2021

Abstract Aims Epidermal growth factor receptor (EGFR) is not only involved in carcinogenesis, but also in chemoresistance. We characterized U87.MGΔEGFR glioblastoma cells with constitutively active EGFR due to deletion at the ligand binding domain in terms of gene expression profiling and chromosomal aberrations. Wild-type U87.MG cells served as control. Materials and methods RNA sequencing and network analyses (Ingenuity Pathway Analysis) were performed to identify novel drug resistance mechanisms related to expression of mutation activated EGFR. Chromosomal aberrations were characterized by multicolor fluorescence in situ hybridization (mFISH) and array comparative genomic hybridization (…

0301 basic medicineDown-RegulationBiologymedicine.disease_cause030226 pharmacology & pharmacyGeneral Biochemistry Genetics and Molecular BiologyTranscriptome03 medical and health sciences0302 clinical medicineCell Line TumormedicineHumansGene Regulatory NetworksProtein Interaction MapsGeneral Pharmacology Toxicology and PharmaceuticsGeneTranscription factorMetaphaseChromosome AberrationsMutationmedicine.diagnostic_testBrain NeoplasmsGene Expression ProfilingGeneral MedicineGenomicsUp-RegulationGene expression profilingErbB ReceptorsGene Expression Regulation Neoplastic030104 developmental biologyDrug Resistance NeoplasmMutationCancer researchCarcinogenesisGlioblastomaTranscriptomeComparative genomic hybridizationFluorescence in situ hybridizationSignal TransductionLife sciences
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MiR-144 overexpression as a promising therapeutic strategy to overcome glioblastoma cell invasiveness and resistance to chemotherapy

2019

Abstract Glioblastoma (GB) is the most aggressive and common form of primary brain tumor, characterized by fast proliferation, high invasion, and resistance to current standard treatment. The average survival rate post-diagnosis is only of 14.6 months, despite the aggressive standard post-surgery treatment approaches of radiotherapy concomitant with chemotherapy with temozolomide. Altered cell metabolism has been identified as an emerging cancer hallmark, including in GB, thus offering a new target for cancer therapies. On the other hand, abnormal expression levels of miRNAs, key regulators of multiple molecular pathways, have been correlated with pathological manifestations of cancer, such…

0301 basic medicineGenetic enhancementmedicine.medical_treatmentBrain tumorAntineoplastic AgentsBiology03 medical and health sciences0302 clinical medicineDownregulation and upregulationCell MovementCell Line TumormicroRNAGeneticsmedicineHumansRNA MessengerU87Molecular BiologyGenetics (clinical)Cell ProliferationTemozolomideBrain NeoplasmsGene Expression ProfilingCancerGeneral Medicinemedicine.disease3. Good healthGene Expression Regulation NeoplasticRadiation therapyMicroRNAs030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchEnergy MetabolismGlioblastomamedicine.drugHuman Molecular Genetics
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Diagnostic implications of intrapatient genetic tumor heterogeneity

2015

The complex genetic composition of neuroblastoma emphasizes the importance of conscientious and meticulous diagnosis. Clones with amplification or segmental chromosomal aberrations sometimes remain hidden. Several determinations should be performed when sufficient tumor material is available to establish the final diagnosis by combining the results of different techniques on tumor fragments or liquid biopsies.

0301 basic medicineGeneticsCancer ResearchBiologymedicine.diseaseTumor heterogeneityIntratumoral Genetic Heterogeneity03 medical and health sciences030104 developmental biology0302 clinical medicine030220 oncology & carcinogenesisNeuroblastomamedicineMolecular MedicineAuthor's ViewGenetic composition
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Molecular bases of the poor response of liver cancer to chemotherapy

2018

Summary A characteristic shared by most frequent types of primary liver cancer, i.e., hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA) in adults, and in a lesser extent hepatoblastoma (HB) mainly in children, is their high refractoriness to chemotherapy. This is the result of synergic interactions among complex and diverse mechanisms of chemoresistance (MOC) in which more than 100 genes are involved. Pharmacological treatment, although it can be initially effective, frequently stimulates the expression of MOC genes, which results in the relapse of the tumor, usually with a more aggressive and less chemosensitive phenotype. Identification of the MOC genetic signature accounting fo…

0301 basic medicineHepatoblastomaCarcinoma HepatocellularGenetic enhancementmedicine.medical_treatmentCholangiocarcinoma03 medical and health sciences0302 clinical medicineHumansMedicinecholangiocarcinoma; hepatoblastoma; hepatocellular carcinoma; multidrug resistance; targeted therapies; hepatology; gastroenterologyChemotherapyHepatologybusiness.industryLiver NeoplasmsGastroenterologymedicine.diseasePhenotypeResistome030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisHepatocellular carcinomaCancer cellCancer researchbusinessLiver cancerClinics and Research in Hepatology and Gastroenterology
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Novel deletion in 11p15.5 imprinting center region 1 in a patient with Beckwith-Wiedemann syndrome provides insight into distal enhancer regulation a…

2016

Background Beckwith–Wiedemann syndrome (BWS) is an early-onset overgrowth disorder with a high risk for embryonal tumors. It is mainly caused by dysregulation of imprinted genes on chromosome 11p15.5; however, the driving forces in the development of tumors are not fully understood. Procedure We report on a female patient presenting with macrosomia, macroglossia, organomegaly and extensive bilateral nephroblastomatosis. Adjuvant chemotherapy was initiated; however, the patient developed hepatoblastoma and Wilms tumor at 5 and 12 months of age, respectively. Subsequent radiofrequency ablation of the liver tumor and partial nephrectomy followed by consolidation therapy achieved complete remis…

0301 basic medicineHepatoblastomaPathologymedicine.medical_specialtyBeckwith-Wiedemann SyndromeBeckwith–Wiedemann syndrome030105 genetics & hereditymedicine.disease_cause03 medical and health sciencesGenomic ImprintingInsulin-Like Growth Factor IIMacroglossiaMedicineHumansImprinting (psychology)NephroblastomatosisSequence Deletionbusiness.industryChromosomes Human Pair 11Infant NewbornWilms' tumorHematologyDNA Methylationmedicine.diseasePrognosis030104 developmental biologyCell Transformation NeoplasticPhenotypeOncologyPediatrics Perinatology and Child HealthCancer researchFemalemedicine.symptombusinessGenomic imprintingCarcinogenesisPediatric bloodcancer
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Epigenetic IVD Tests for Personalized Precision Medicine in Cancer

2019

Epigenetic alterations play a key role in the initiation and progression of cancer. Therefore, it is possible to use epigenetic marks as biomarkers for predictive and precision medicine in cancer. Precision medicine is poised to impact clinical practice, patients, and healthcare systems. The objective of this review is to provide an overview of the epigenetic testing landscape in cancer by examining commercially available epigenetic-based in vitro diagnostic tests for colon, breast, cervical, glioblastoma, lung cancers, and for cancers of unknown origin. We compile current commercial epigenetic tests based on epigenetic biomarkers (i.e., DNA methylation, miRNAs, and histones) that can actua…

0301 basic medicineIn Vitro Diagnostic (IVD)lcsh:QH426-470precision medicineReviewBioinformatics03 medical and health sciences0302 clinical medicinemicroRNAGeneticsMedicineEpigeneticscfDNAGenetics (clinical)miRNAEpigenetic biomarkersDNA methylationbiologybusiness.industryCancerepigenetic biomarkerPrecision medicinemedicine.diseaselcsh:Genetics030104 developmental biologyHistone030220 oncology & carcinogenesisDNA methylationcirculating nucleosomesbiology.proteinMolecular MedicinebusinessGlioblastomaFrontiers in Genetics
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Polysialic acid chains exhibit enhanced affinity for ordered regions of membranes.

2018

Polysialic acid (polySia) forms linear chains which are usually attached to the external surface of the plasma membrane mainly through the Neural Cell Adhesion Molecule (NCAM) protein. It is exposed on neural cells, several types of cancer cells, dendritic cells, and egg and sperm cells. There are several lipid raft-related phenomena in which polySia is involved; however the mechanisms of polySia action as well as determinants of its localization in lipid raft microdomains are still unknown, although the majority of NCAM molecules in the liquid-ordered raft membrane fractions of neural cells appear to be polysialylated. Here we investigate the affinity of polySia (both soluble and NCAM-depe…

0301 basic medicineLipid BilayersBiophysicsPolysialic acidBiochemistryGiant vesicles03 medical and health sciencesNeuroblastomaRafts0302 clinical medicineMembrane MicrodomainsCell Line TumorNeuroblastoma cellsFluorescence Resonance Energy TransferHumansLipid raftNeuronsLiposomePolysialic acidChemistryCell MembraneCell BiologyRaftLipidsKinetics030104 developmental biologyMembraneFörster resonance energy transferMicroscopy FluorescenceSolubilityCancer cellLiposomesFRETBiophysicsSialic AcidsNeural cell adhesion molecule030217 neurology & neurosurgeryProtein BindingBiochimica et biophysica acta. Biomembranes
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