Search results for " p53"

showing 10 items of 252 documents

Contribution of allelic imbalance to colorectal cancer

2018

Point mutations in cancer have been extensively studied but chromosomal gains and losses have been more challenging to interpret due to their unspecific nature. Here we examine high-resolution allelic imbalance (AI) landscape in 1699 colorectal cancers, 256 of which have been whole-genome sequenced (WGSed). The imbalances pinpoint 38 genes as plausible AI targets based on previous knowledge. Unbiased CRISPR-Cas9 knockout and activation screens identified in total 79 genes within AI peaks regulating cell growth. Genetic and functional data implicate loss of TP53 as a sufficient driver of AI. The WGS highlights an influence of copy number aberrations on the rate of detected somatic point muta…

0301 basic medicineDenmarkLoss of HeterozygosityGeneral Physics and AstronomyAllelic ImbalanceLoss of heterozygosityGenotypeddc:576.5RNA Small Interferinglcsh:ScienceRNA Small Interfering/geneticsGeneticsMultidisciplinaryQGenomicsPhenotype3. Good healthGENOMEPhenotypesyöpägeenitAllelic ImbalanceTumor Suppressor Protein p53/geneticsColorectal NeoplasmsChromosomes Human Pair 8GENESDNA Copy Number VariationsGenotypeScienceTranscription Factors/geneticsGenomicscolorectal cancerBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins p21(ras)Proto-Oncogene Proteins p21(ras)/genetics03 medical and health sciencesmedicineHumansPoint MutationGenetic Predisposition to DiseaseGenepaksusuolisyöpäChromosome AberrationsWhole Genome SequencingHUMAN-COLONGene Expression ProfilingPoint mutationCancerGeneral Chemistrymedicine.diseaseColorectal Neoplasms/geneticsENHANCERS030104 developmental biologyCELLSlcsh:Q3111 BiomedicineTumor Suppressor Protein p53CRISPR-Cas SystemsmutaatiotTranscription FactorsMicrosatellite Repeats
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Effects of mutations in Wnt/β-catenin, hedgehog, Notch and PI3K pathways on GSK-3 activity—Diverse effects on cell growth, metabolism and cancer

2016

Glycogen synthase kinase-3 (GSK-3) is a serine/threonine kinase that participates in an array of critical cellular processes. GSK-3 was first characterized as an enzyme that phosphorylated and inactivated glycogen synthase. However, subsequent studies have revealed that this moon-lighting protein is involved in numerous signaling pathways that regulate not only metabolism but also have roles in: apoptosis, cell cycle progression, cell renewal, differentiation, embryogenesis, migration, regulation of gene transcription, stem cell biology and survival. In this review, we will discuss the roles that GSK-3 plays in various diseases as well as how this pivotal kinase interacts with multiple sign…

0301 basic medicineMAPK/ERK pathwaySettore MED/06 - Oncologia MedicaCellular differentiationPI3KTargeted therapyGlycogen Synthase Kinase 3Phosphatidylinositol 3-Kinases0302 clinical medicineGSK-3Neoplasmsbeta CateninGSK-3biologyReceptors NotchKinaseWnt signaling pathwayWnt/beta-cateninCell DifferentiationCell biologyGene Expression Regulation Neoplastic030220 oncology & carcinogenesismTORAkt; GSK-3; Hedgehog; Notch; PI3K; Targeted therapy; Therapy resistance; Wnt/beta-catenin; mTORSignal TransductionBeta-cateninNotchAkt GSK-3 Hedgehog mTOR Notch PI3K Targeted therapy Therapy resistance Wnt/beta-cateninCell Survivalmacromolecular substancesNO03 medical and health sciencesAkt; GSK-3 Hedgehog Notch PI3K Targeted therapy Therapy resistance Wnt/beta-catenin mTORAnimalsHumansHedgehog ProteinsProtein kinase BMolecular BiologyPI3K/AKT/mTOR pathwayCell ProliferationAktTherapy resistanceAkt; GSK-3; Hedgehog; mTOR; Notch; PI3K; Targeted therapy; Therapy resistance; Wnt/beta-catenin; Molecular Biology; Cell BiologyCell BiologyWnt ProteinsMicroRNAs030104 developmental biologyMutationCancer researchbiology.proteinTumor Suppressor Protein p53Hedgehog
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Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.

2019

Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of…

0301 basic medicineMaleCancer ResearchBiopsyL-amp GB EGFR-low amplified glioblastomamedicine.disease_causewt wildtypeMYBPC3 myosin-binding protein C0302 clinical medicineHIC1 hypermethylated in cancer 1Gene duplicationIn Situ Hybridization FluorescenceIDH2 isocitrate dehydrogenase 2MutationRB-pat RB signaling pathwayEGFRvIII epidermal growth factor receptor variant number IIIPAH phenylalanine hydroxylaseGBM glioblastoma IDH-wildtype (glioblastoma multiforme primary glioblastoma).ANOVA ANalysis Of VArianceN-amp GB EGFR-no amplified glioblastomaMiddle AgedCDKN2A cyclin-dependent kinase inhibitor 2Alcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisPrimary tumorImmunohistochemistryH-amp GB EGFR-high amplified glioblastomaErbB ReceptorsTKR-pat tyrosine-kinase receptors signaling pathway030220 oncology & carcinogenesisDisease ProgressionCDK6 cyclin-dependent kinase 6CDH1 Cadherin 1FemaleCREM cAMP response element modulatorIHC immunohistochemistryAdultOriginal articleDNA Copy Number VariationsCDKN1B cyclin-dependent kinase inhibitor 1BBiologyRARB retinoic acid receptor betaCNS central nervous systemlcsh:RC254-282IDH1 isocitrate dehydrogenase 1BCL2 B-cell cll/ lymphoma 2CNAs copy number algerationsWHO World Health Organization03 medical and health sciencesYoung Adultp53-pat p53 signaling pathwaymedicineBiomarkers TumorTMA tissue microarrayPTENHumansProtein kinase BPI3K/AKT/mTOR pathwaySurvival analysisAgedGenetic heterogeneityGene AmplificationGFAP glial fibrillary acidic proteinMLPA multiplex ligation-dependent probe amplificationmedicine.diseaseFISH fluorescence in situ hibridizationSurvival AnalysisCDKN2B cyclin-dependent kinase inhibitor 2BPTEN phosphatase and tensin homologEGFR epidermal growth factor receptorCNV-load load of copy number variations030104 developmental biologyMutationPARK2 parkinCancer researchbiology.proteinTCGA The Cancer Genome AtlasLARGE1 acetylglucosaminyltransferase-like protein 1GlioblastomaCHD7 Chromodomain Helicase DNA Binding Protein 7DAPI 4′6-diamidino-2-phenylindoleNeoplasia (New York, N.Y.)
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Ibrutinib, obinutuzumab, and venetoclax in relapsed and untreated patients with mantle cell lymphoma: a phase 1/2 trial.

2020

Abstract Ibrutinib, obinutuzumab, and venetoclax demonstrate synergy in preclinical models of mantle cell lymphoma (MCL). OAsIs (NCT02558816), a single-arm multicenter prospective phase 1/2 trial, aimed to determine the maximum tolerated dose of venetoclax in combination with fixed doses of ibrutinib and obinutuzumab, in relapsed MCL patients. At the venetoclax MTD, extension cohorts were opened for relapsed and untreated patients. Safety and efficacy were secondary objectives. Minimal residual disease (MRD) was assessed by allele-specific oligonucleotide quantitative polymerase chain reaction. Between 14 October 2015 and 29 May 2018, 48 patients were enrolled. No dose-limiting toxicity was…

0301 basic medicineMaleNeoplasm Residualmedicine.medical_treatmentImmunoglobulin Variable RegionHematopoietic stem cell transplantationKaplan-Meier EstimateLymphoma Mantle-CellBiochemistryGastroenterologychemistry.chemical_compound0302 clinical medicinePiperidinesObinutuzumabAntineoplastic Combined Chemotherapy ProtocolsProspective StudiesProspective cohort studyAged 80 and overSulfonamidesHematopoietic Stem Cell TransplantationHematologyMiddle AgedCombined Modality TherapyProgression-Free Survival3. Good healthTreatment Outcome030220 oncology & carcinogenesisIbrutinibFemaleImmunoglobulin Heavy Chainsmedicine.medical_specialtyMaximum Tolerated DoseImmunologyAntibodies Monoclonal Humanized03 medical and health sciencesInternal medicinemedicineHumansProgression-free survivalAgedVenetoclaxbusiness.industryAdenineCell Biologymedicine.diseaseBridged Bicyclo Compounds HeterocyclicGenes p53Minimal residual diseaseHematologic Diseases030104 developmental biologychemistryMutationMantle cell lymphomabusinessFollow-Up StudiesBlood
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The unbalanced p53/SIRT1 axis may impact lymphocyte homeostasis in COVID-19 patients

2021

Abstract Background/objectives A dysregulated inflammatory profile plays an important role in coronavirus disease-2019 (COVID-19) pathogenesis. Moreover, the depletion of lymphocytes is typically associated with an unfavourable disease course. We studied the role and impact of p53 and deacetylase Sirtuin 1 (SIRT1) on lymph-monocyte homeostasis and their possible effect on T and B cell signalling. Methods Gene expression analysis and flow cytometry were performed on peripheral blood mononuclear cells (PBMC) of 35 COVID-19 patients and 10 healthy donors (HD). Inflammatory cytokines, the frequency of Annexin+ cells among CD3+ T cells and CD19+ B cell subsets were quantified. Results PBMC from …

0301 basic medicineMicrobiology (medical)Male030106 microbiologyInflammationInfectious and parasitic diseasesRC109-216CD19ArticleProinflammatory cytokineBLNK Inflammation03 medical and health sciences0302 clinical medicineSirtuin 1Lymphocyte homeostasismedicineHomeostasisHumans030212 general & internal medicineLymphocytesInterleukin-7 receptorB cellAgedInflammationBLNKbiologySirtuin 1SARS-CoV-2COVID-19p53/SIRT1General MedicineIL-7RMiddle Agedmedicine.anatomical_structureInfectious DiseasesSettore MED/38 - PEDIATRIA GENERALE E SPECIALISTICABLNK; COVID-19; IL-7R; inflammation; p53/SIRT1ImmunologyB-cell linkerbiology.proteinCytokinesFemalemedicine.symptomTumor Suppressor Protein p53
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The EP300/TP53 pathway, a suppressor of the Hippo and canonical WNT pathways, is activated in human hearts with arrhythmogenic cardiomyopathy in the …

2021

Aim Arrhythmogenic cardiomyopathy (ACM) is a primary myocardial disease that typically manifests with cardiac arrhythmias, progressive heart failure and sudden cardiac death (SCD). ACM is mainly caused by mutations in genes encoding desmosome proteins. Desmosomes are cell-cell adhesion structures and hubs for mechanosensing and mechanotransduction. The objective was to identify the dysregulated molecular and biological pathways in human ACM in the absence of overt heart failure. Methods and results Transcriptomes in the right ventricular endomyocardial biopsy samples from three independent individuals carrying truncating mutations in the DSP gene and 5 control samples were analyzed by RNA-S…

0301 basic medicinePhysiologyCardiomyopathy030204 cardiovascular system & hematologyBiologyMechanotransduction CellularBiological pathway03 medical and health sciences0302 clinical medicinePhysiology (medical)medicineHumansMechanotransductionEP300Wnt Signaling PathwayArrhythmogenic Right Ventricular DysplasiaHeart FailureHippo signaling pathwayWnt signaling pathwayArrhythmias CardiacOriginal Articlesmedicine.diseaseCell biologyDeath Sudden Cardiac030104 developmental biologyCardiomyopathy Gene expression Hippo pathway RNA-Sequencing TP53 WNT pathwayHeart failureTumor Suppressor Protein p53Signal transductionCardiomyopathiesCardiology and Cardiovascular MedicineE1A-Associated p300 ProteinCardiovascular Research
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Enzymatic Spermine Metabolites Induce Apoptosis Associated with Increase of p53, caspase-3 and miR-34a in Both Neuroblastoma Cells, SJNKP and the N-M…

2021

Neuroblastoma (NB) is a common malignant solid tumor in children and accounts for 15% of childhood cancer mortality. Amplification of the N-Myc oncogene is a well-established poor prognostic marker in NB patients and strongly correlates with higher tumor aggression and resistance to treatment. New therapies for patients with N-Myc-amplified NB need to be developed. After treating NB cells with BSAO/SPM, the detection of apoptosis was determined after annexin V-FITC labeling and DNA staining with propidium iodide. The mitochondrial membrane potential activity was checked, labeling cells with the probe JC-1 dye. We analyzed, by real-time RT-PCR, the transcript of genes involved in the apoptot…

0301 basic medicinePolyamine; neuroblastoma; apoptosis; microRNA; mitochondria; reactive oxygen species; oncotherapychemistry.chemical_compound0302 clinical medicineAnnexinpolyamineSettore BIO/10 - BiochimicaAntineoplastic Combined Chemotherapy ProtocolsCytotoxic T cellSettore BIO/06 - Anatomia Comparata E CitologiaBiology (General)Membrane Potential Mitochondrialreactive oxygen speciesN-Myc Proto-Oncogene ProteinmicroRNAChemistryCaspase 3apoptosisGeneral MedicineBlotGene Expression Regulation Neoplasticmitochondria030220 oncology & carcinogenesisAmine Oxidase (Copper-Containing)Signal TransductiononcotherapyQH301-705.5Caspase 3apoptosis; microRNA; mitochondria; neuroblastoma; oncotherapy; polyamine; reactive oxygen species.ArticleNO03 medical and health sciencesneuroblastomaNeuroblastomaCell Line TumormedicineAnimalsHumansPropidium iodideRats WistarCell ProliferationOncogeneGene Amplificationmedicine.diseaseapoptosis; microRNA; mitochondria; neuroblastoma; oncotherapy; polyamine; reactive oxygen speciesMolecular biologyMicroRNAs030104 developmental biologyApoptosisSpermineTumor Suppressor Protein p53
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p53 and p53-related mediators PAI-1 and IGFBP-3 are downregulated in peripheral blood mononuclear cells of HIV-patients exposed to non-nucleoside rev…

2019

The improved effectiveness and safety of the combined antiretroviral therapy (cART) has largely diminished mortality and AIDS-defining morbidity of HIV-patients. Nevertheless, chronic age-related diseases in these individuals are more common and their underlying pathogenic mechanisms of these actions seem to involve accelerated aging and enhanced inflammation. The present study explores markers of these processes in a heterogenous Spanish HIV cohort using peripheral blood samples of HIV-patients and matched uninfected controls. We isolated periheral blood mononuclear cells (PBMCs) and i) compared the expression of a panel of 14 genes related to inflammation and senescence in PBMCs of HIV-pa…

0301 basic medicineSenescenceAdultMaleAnti-HIV Agents030106 microbiologyDown-RegulationInflammationHIV InfectionsCCL2Peripheral blood mononuclear cell03 medical and health sciencesVirologyAntiretroviral Therapy Highly ActivePlasminogen Activator Inhibitor 1medicineCXCL10HumansCellular SenescencePharmacologyInflammationbusiness.industryInterleukin-6Interleukin-18virus diseasesMiddle AgedCCL20Chemokine CXCL10030104 developmental biologyInsulin-Like Growth Factor Binding Protein 3ImmunologyLeukocytes MononuclearReverse Transcriptase InhibitorsInterleukin 18Tumor necrosis factor alphaFemalemedicine.symptomTumor Suppressor Protein p53businessAntiviral research
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Vascular ageing and endothelial cell senescence: Molecular mechanisms of physiology and diseases

2016

Ageing leads to a progressive deterioration of structure and function of all organs over the time. During this process endothelial cells undergo senescence and manifest significant changes in their properties, resulting in impairment of the vascular functionality and neo-angiogenic capability. This ageing-dependent impairment of endothelial functions is considered a key factor contributing to vascular dysfunctions, which is responsible of several age-related diseases of the vascular system and other organs. Several mechanisms have been described to control ageing-related endothelial cell senescence including microRNAs, mitochondrial dysfunction and micro environmental stressors, such as hyp…

0301 basic medicineSenescenceAgingEndotheliump73Biologymedicine.disease_cause03 medical and health sciencesEndotheliocyte; Endothelium; Hypoxia; MicroRNAs; Mitochondrial dysfunction; Oxidative stress; P53 family; P73; Transglutaminase 2; VEGF; Aging; Developmental BiologymicroRNAmedicineAnimalsHumansSettore MED/05 - Patologia ClinicaEndotheliocyte; Endothelium; Hypoxia; Mitochondrial dysfunction; Oxidative stress; Transglutaminase 2; VEGF; microRNAs; p53 family; p73Vascular DiseasesEndotheliumHypoxiaCellular SenescenceEndothelial CellsMicroRNASettore MED/23 - Chirurgia CardiacaBECN1Hypoxia (medical)VEGFMitochondriamicroRNAsEndothelial stem cellTransglutaminase 2030104 developmental biologymedicine.anatomical_structureOxidative stressAgeingImmunologyOxidative stremedicine.symptomMitochondrial dysfunctionp53 familyEndotheliocyteNeuroscienceOxidative stressDevelopmental BiologyMechanisms of Ageing and Development
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Telomeres and Telomerase During Human Papillomavirus-Induced Carcinogenesis

2018

Human papillomaviruses (HPVs) belong to a small spherical virus family and are transmitted through direct contact, most often through sexual behavior. More than 200 types of HPV are known, a dozen or so of which are classified as high-risk viruses (HR HPV) and may contribute to the development of cervical cancer. HPV is a small virus with a capsid composed of L1 and L2 proteins, which are crucial for entry to the cell. The infection begins at the basal cell layer and progresses to involve cells from higher layers of the cervical epithelium. E6 and E7 viral proteins are involved in the process of carcinogenesis. They interact with suppressors of oncogenesis, including p53 and Rb proteins. Th…

0301 basic medicineTelomeraseOncogene ProteinsCarcinogenesisCellReview ArticleBiologymedicine.disease_causeRetinoblastoma ProteinVirus03 medical and health sciences0302 clinical medicineGeneticsmedicineHumansTelomerase reverse transcriptasePapillomaviridaeTelomeraseTelomere ShorteningPharmacologyPapillomavirus InfectionsDNA replicationGeneral MedicineOncogene Proteins ViralVirus InternalizationCell Transformation ViralTelomere030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisCancer researchDisease ProgressionMolecular MedicineRNAFemaleTumor Suppressor Protein p53CarcinogenesisMolecular Diagnosis & Therapy
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