Search results for "P53"

showing 10 items of 303 documents

Impact of somatic mutations in myelodysplastic patients with isolated partial or total loss of chromosome 7

2020

Monosomy 7 [-7] and/or partial loss of chromosome 7 [del(7q)] are associated with poor and intermediate prognosis, respectively, in myelodysplastic syndromes (MDS), but somatic mutations may also play a key complementary role. We analyzed the impact on the outcomes of deep targeted mutational screening in 280 MDS patients with -7/del(7q) as isolated cytogenetic abnormality (86 with del(7q) and 194 with -7). Patients with del(7q) or -7 had similar demographic and disease-related characteristics. Somatic mutations were detected in 79% (93/117) of patients (82% in -7 and 73% in del(7q) group). Median number of mutations per patient was 2 (range 0-8). There was no difference in mutation frequen…

0301 basic medicineAdultMalemyelodysplastic syndromes chromosome abnormalities prognosisCancer Researchmedicine.medical_specialtyAdolescentSomatic cellTp53 mutationGastroenterology03 medical and health sciences0302 clinical medicinePartial lossCytogenetic AbnormalityInternal medicineAntineoplastic Combined Chemotherapy ProtocolsMedicineHumansMutation frequencyAgedChromosome 7 (human)Aged 80 and overbusiness.industryMyelodysplastic syndromesHematologyMiddle Agedmedicine.diseasePrognosisSurvival AnalysisMutational analysis030104 developmental biologyOncology030220 oncology & carcinogenesisMyelodysplastic SyndromesMutationFemaleChromosome DeletionbusinessChromosomes Human Pair 7
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Theabrownin triggersDNAdamage to suppress human osteosarcoma U2OScells by activating p53 signalling pathway

2018

Abstract Osteosarcoma becomes the second leading cause of cancer death in the younger population. Current outcomes of chemotherapy on osteosarcoma were unsatisfactory to date, demanding development of effective therapies. Tea is a commonly used beverage beneficial to human health. As a major component of tea, theabrownin has been reported to possess anti‐cancer activity. To evaluate its anti‐osteosarcoma effect, we established a xenograft model of zebrafish and employed U2OS cells for in vivo and in vitro assays. The animal data showed that TB significantly inhibited the tumour growth with stronger effect than that of chemotherapy. The cellular data confirmed that TB‐triggered DNA damage an…

0301 basic medicineApoptosisCatechinHistones0302 clinical medicineRNA Small InterferingZebrafisheducation.field_of_studyCaspase 3ChemistryCell CycleGene Expression Regulation NeoplasticLarva030220 oncology & carcinogenesisMolecular MedicineOsteosarcomaOriginal ArticlePoly(ADP-ribose) PolymerasesSignal TransductionCell SurvivalDNA damagePoly ADP ribose polymerasePopulationBone NeoplasmsCaspase 303 medical and health sciencesAnimal dataosteosarcomaCell Line TumormedicineAnimalsHumanstheabrownineducationP53OsteoblastsMesenchymal Stem CellsOriginal ArticlesCell Biologymedicine.diseaseAntineoplastic Agents PhytogenicXenograft Model Antitumor AssaysKi-67 Antigen030104 developmental biologyApoptosisCell cultureCancer researchDNA damageCisplatinTumor Suppressor Protein p53Journal of Cellular and Molecular Medicine
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Mutant p53 induces Golgi tubulo-vesiculation driving a prometastatic secretome

2020

TP53 missense mutations leading to the expression of mutant p53 oncoproteins are frequent driver events during tumorigenesis. p53 mutants promote tumor growth, metastasis and chemoresistance by affecting fundamental cellular pathways and functions. Here, we demonstrate that p53 mutants modify structure and function of the Golgi apparatus, culminating in the increased release of a pro-malignant secretome by tumor cells and primary fibroblasts from patients with Li-Fraumeni cancer predisposition syndrome. Mechanistically, interacting with the hypoxia responsive factor HIF1α, mutant p53 induces the expression of miR-30d, which in turn causes tubulo-vesiculation of the Golgi apparatus, leading …

0301 basic medicineBiopsyGeneral Physics and AstronomyGolgi ApparatusAnimals Biopsy Breast Neoplasms Cell Line Tumor Cell Transformation Neoplastic Female Fibroblasts Gene Expression Regulation Neoplastic Golgi Apparatus Humans Hypoxia-Inducible Factor 1 alpha Subunit Li-Fraumeni Syndrome Mice MicroRNAs Microtubules Mutation Primary Cell Culture Secretory Vesicles Signal TransductionSkin Tumor Microenvironment Tumor Suppressor Protein p53 Xenograft Model Antitumor Assays02 engineering and technologymedicine.disease_causeCell TransformationMicrotubulesSettore BIO/09 - FisiologiaMetastasisLi-Fraumeni SyndromeMiceTumor MicroenvironmentGolgisecretory machinerySuper-resolution microscopyAnimals; Biopsy; Breast Neoplasms; Cell Line Tumor; Cell Transformation Neoplastic; Female; Fibroblasts; Gene Expression Regulation Neoplastic; Golgi Apparatus; Humans; Hypoxia-Inducible Factor 1 alpha Subunit; Li-Fraumeni Syndrome; Mice; MicroRNAs; Microtubules; Mutation; Primary Cell Culture; Secretory Vesicles; Signal Transduction; Skin; Tumor Microenvironment; Tumor Suppressor Protein p53; Xenograft Model Antitumor Assayslcsh:ScienceSkinMultidisciplinaryTumorChemistrymutant p53QCell migrationMicroRNASecretomics021001 nanoscience & nanotechnologyCell biologyGene Expression Regulation NeoplasticCell Transformation NeoplasticsymbolsFibroblastmiR-30dFemaleHypoxia-Inducible Factor 10210 nano-technologyBreast NeoplasmHumanSignal TransductionCancer microenvironmentStromal cellSecretory VesicleSciencePrimary Cell CultureBreast NeoplasmsMicrotubuleGolgi ApparatuSettore MED/08 - Anatomia Patologicaalpha SubunitGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencessymbols.namesakeCell Line TumormedicineAnimalsHumansSettore MED/05 - Patologia ClinicaSecretionTumor microenvironmentNeoplasticAnimalSecretory VesiclesGeneral ChemistryOncogenesGolgi apparatusHDAC6FibroblastsMicroreviewHypoxia-Inducible Factor 1 alpha SubunitmicroenvironmentXenograft Model Antitumor AssaysMicroRNAs030104 developmental biologyGene Expression RegulationMutationlcsh:QTumor Suppressor Protein p53Carcinogenesis
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Knockdown of hnRNPK leads to increased DNA damage after irradiation and reduces survival of tumor cells.

2017

Radiotherapy is an important treatment option in the therapy of multiple tumor entities among them head and neck squamous cell carcinoma (HNSCC). However, the success of radiotherapy is limited by the development of radiation resistances. Heterogeneous nuclear ribonucleoprotein K (hnRNPK) is a cofactor of p53 and represents a potential target for radio sensitization of tumor cells. In this study, we analyzed the impact of hnRNPK on the DNA damage response after gamma irradiation. By yH2AX foci analysis, we found that hnRNPK knockdown increases DNA damage levels in irradiated cells. Tumor cells bearing a p53 mutation showed increased damage levels and delayed repair. Knockdown of hnRNPK appl…

0301 basic medicineCancer ResearchDNA damageCell Survivalmedicine.medical_treatmentmedicine.disease_causeRadiation ToleranceHeterogeneous-Nuclear Ribonucleoprotein KHistones03 medical and health sciences0302 clinical medicineCell Line TumormedicineCarcinomaGene Knockdown TechniquesHumansMutationGene knockdownChemistrySquamous Cell Carcinoma of Head and NeckStem CellsGeneral Medicinemedicine.diseaseHead and neck squamous-cell carcinomaRadiation therapy030104 developmental biologyCell cultureHead and Neck Neoplasms030220 oncology & carcinogenesisGene Knockdown TechniquesCancer researchCarcinoma Squamous CellTumor Suppressor Protein p53DNA DamageCarcinogenesis
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Doxorubicin anti-tumor mechanisms include Hsp60 post-translational modifications leading to the Hsp60/p53 complex dissociation and instauration of re…

2017

Hsp60 is a pro-carcinogenic chaperonin in certain tumor types by interfering with apoptosis and with tumor cell death. In these tumors, it is not known whether or not doxorubicin anti-tumor effects include a blockage of the pro-carcinogenic action of this protein. We used the human lung mucoepidermoid cell line NCI-H292 and different doses of doxorubicin to measure cell viability, cell cycle progression, cell senescence indicators, Hsp60 levels and its post-translational modifications as well as the release of the chaperonin into the extracellular environment. Cell viability was reduced in relation to doxorubicin dose and this was paralleled by the appearance of cell senescence markers. Con…

0301 basic medicineCancer ResearchLung NeoplasmsChaperoninsCellApoptosismedicine.disease_causeHistones0302 clinical medicineCellular SenescenceAntibiotics AntineoplasticAcetylationG2 Phase Cell Cycle Checkpointsmedicine.anatomical_structureOncology030220 oncology & carcinogenesisCell agingIntracellularProtein BindingSignal TransductionSenescenceCyclin-Dependent Kinase Inhibitor p21animal structuresCell Survivalchemical and pharmacologic phenomenaBiologycomplex mixturesMitochondrial ProteinsDoxorubicin Hsp60 Acetylation Ubiquitination p53 Replicative senescence03 medical and health sciencesDoxorubicin; Hsp60; p53; replicative senescence; post-translational modificationsCell Line TumormedicineHumansCell Proliferationdoxorubicin p53 Hsp60Dose-Response Relationship DrugCell growthfungiUbiquitinationChaperonin 60Molecular biology030104 developmental biologyAcetylationApoptosisDoxorubicinProteolysisCancer researchCarcinoma MucoepidermoidTumor Suppressor Protein p53CarcinogenesisProtein Processing Post-Translational
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Trabectedin Overrides Osteosarcoma Differentiative Block and Reprograms the Tumor Immune Environment Enabling Effective Combination with Immune Check…

2016

Abstract Purpose: Osteosarcoma, the most common primary bone tumor, is characterized by an aggressive behavior with high tendency to develop lung metastases as well as by multiple genetic aberrations that have hindered the development of targeted therapies. New therapeutic approaches are urgently needed; however, novel combinations with immunotherapies and checkpoint inhibitors require suitable preclinical models with intact immune systems to be properly tested. Experimental Design: We have developed immunocompetent osteosarcoma models that grow orthotopically in the bone and spontaneously metastasize to the lungs, mimicking human osteosarcoma. These models have been used to test the effica…

0301 basic medicineCancer ResearchLung Neoplasmsmedicine.medical_treatmentCellular differentiationT-LymphocytesProgrammed Cell Death 1 ReceptorBone NeoplasmsCore Binding Factor Alpha 1 SubunitDioxolesBiology03 medical and health sciences0302 clinical medicineImmune systemCell Line TumorTetrahydroisoquinolinesmedicineTumor MicroenvironmentHumansTrabectedinTumor microenvironmentOsteosarcomaCancerCell DifferentiationImmunotherapymedicine.diseaseCellular ReprogrammingPrimary tumor030104 developmental biologyOncology030220 oncology & carcinogenesisImmunologyCancer researchOsteosarcomaImmunotherapyOsteosarcoma Trabectedin tumor mouse models immune cells immune checkpoint inhibitors.Tumor Suppressor Protein p53medicine.drugTrabectedinClinical cancer research : an official journal of the American Association for Cancer Research
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Effects of the MDM-2 inhibitor Nutlin-3a on PDAC cells containing and lacking WT-TP53 on sensitivity to chemotherapy, signal transduction inhibitors …

2019

Abstract Mutations at the TP53 gene are readily detected (approximately 50–75%) in pancreatic ductal adenocarcinoma (PDAC) patients. TP53 was previously thought to be a difficult target as it is often mutated, deleted or inactivated on both chromosomes in certain cancers. In the following study, the effects of restoration of wild-type (WT) TP53 activity on the sensitivities of MIA-PaCa-2 pancreatic cancer cells to the MDM2 inhibitor nutlin-3a in combination with chemotherapy, targeted therapy, as well as, nutraceuticals were examined. Upon introduction of the WT-TP53 gene into MIA-PaCa-2 cells, which contain a TP53 gain of function (GOF) mutation, the sensitivity to the MDM2 inhibitor incre…

0301 basic medicineCancer ResearchNutlin-3aSettore MED/09 - Medicina Internaendocrine system diseasesmedicine.medical_treatmentmedicine.disease_causePiperazinesTargeted therapy0302 clinical medicineTP53MutationbiologyChemistryImidazolesProto-Oncogene Proteins c-mdm2OxaliplatinTargeted TherapeuticsDrug sensitivity; Nutlin-3a; Nutraceuticals; Targeted therapeutics; TP53030220 oncology & carcinogenesisMolecular MedicineMdm2NutraceuticalNutraceuticalsSignal transductionCarcinoma Pancreatic DuctalSignal Transductionmedicine.drugDrug sensitivityAntineoplastic AgentsIrinotecan03 medical and health sciencesCell Line TumorPancreatic cancerGeneticsmedicineHumansMolecular BiologyneoplasmsChemotherapymedicine.diseasedigestive system diseasesOxaliplatinPancreatic Neoplasms030104 developmental biologyCell cultureDietary Supplementsbiology.proteinCancer researchTERAPÊUTICA MÉDICATumor Suppressor Protein p53
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Introduction of WT-TP53 into pancreatic cancer cells alters sensitivity to chemotherapeutic drugs, targeted therapeutics and nutraceuticals

2018

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive, highly metastatic malignancy and accounts for 85% of pancreatic cancers. PDAC patients have poor prognosis with a five-year survival of only 5–10%. Mutations at the TP53 gene are readily detected in pancreatic tumors isolated from PDAC patients. We have investigated the effects of restoration of wild-type (WT) TP53 activity on the sensitivity of pancreatic cancer cells to: chemotherapy, targeted therapy, as well as, nutraceuticals. Upon introduction of the WT-TP53 gene into the MIA-PaCa-2 pancreatic cancer cell line, the sensitivity to drugs used to treat pancreatic cancer cells such as: gemcitabine, fluorouracil (5FU), cisp…

0301 basic medicineCancer ResearchPaclitaxelendocrine system diseasesmedicine.medical_treatmentTargeted therapeuticIrinotecanDeoxycytidineTargeted therapyGlycogen Synthase Kinase 303 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorPancreatic cancerGeneticsmedicineHumansDoxorubicinTP53Signal transduction inhibitorneoplasmsMolecular BiologyCell ProliferationCisplatinChemotherapybusiness.industryPancreatic Neoplasmmedicine.diseaseGemcitabinedigestive system diseasesGemcitabinePancreatic NeoplasmsOxaliplatin030104 developmental biologyPaclitaxelchemistryFluorouracil030220 oncology & carcinogenesisCancer researchMolecular MedicineFluorouracilCisplatinbusinessDrug sensitivityHumanSignal Transductionmedicine.drug
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HDAC1 and HDAC2 integrate the expression of p53 mutants in pancreatic cancer.

2015

Mutation of p53 is a frequent genetic lesion in pancreatic cancer being an unmet clinical challenge. Mutants of p53 have lost the tumour-suppressive functions of wild type p53. In addition, p53 mutants exert tumour-promoting functions, qualifying them as important therapeutic targets. Here, we show that the class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of p53 mutants in human and genetically defined murine pancreatic cancer cells. Our data reveal that the inhibition of these HDACs with small molecule HDAC inhibitors (HDACi), as well as the specific genetic elimination of HDAC1 and HDAC2, reduce the expression of mutant p53 mRNA and protein levels. We fur…

0301 basic medicineCancer ResearchProteasome Endopeptidase ComplexMutantHistone Deacetylase 2Histone Deacetylase 1Biologymedicine.disease_causeMolecular oncologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicePancreatic cancerGeneticsmedicineAnimalsHumansRNA MessengerPromoter Regions GeneticMolecular BiologyRegulation of gene expressionMice KnockoutMutationWild typeCancerProto-Oncogene Proteins c-mdm2medicine.diseaseGenes p53HDAC13. Good healthGene Expression Regulation NeoplasticHistone Deacetylase InhibitorsPancreatic NeoplasmsDisease Models Animal030104 developmental biologyMutationCancer researchOncogene
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Abilities of berberine and chemically modified berberines to interact with metformin and inhibit proliferation of pancreatic cancer cells.

2019

Abstract Pancreatic cancer is devastating cancer worldwide with few if any truly effective therapies. Pancreatic cancer has an increasing incidence and may become the second leading cause of death from cancer. Novel, more effective therapeutic approaches are needed as pancreatic cancer patients usually survive for less than a year after being diagnosed. Control of blood sugar levels by the prescription drug metformin in diseases such as diabetes mellitus has been examined in association with pancreatic cancer. While the clinical trials remain inconclusive, there is hope that certain diets and medications may affect positively the outcomes of patients with pancreatic and other cancers. Other…

0301 basic medicineCancer ResearchSettore MED/09 - Medicina Internaendocrine system diseasesBerberineSignal transduction inhibitorsBlood sugarPharmacologyAMP-Activated Protein KinasesBerberine; PDAC; Signal transduction inhibitors; TP5303 medical and health scienceschemistry.chemical_compound0302 clinical medicineBerberineMETFORMINAPancreatic cancerDiabetes mellitusGeneticsmedicineHumansTP53Signal transduction inhibitorMolecular BiologyCell Proliferationbusiness.industryPDACCancerAMPKmedicine.diseaseMetforminMetforminNeoplasm ProteinsPancreatic Neoplasms030104 developmental biologychemistry030220 oncology & carcinogenesisCancer cellMolecular Medicinebusinessmedicine.drugAdvances in biological regulation
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