Search results for "tp53"

showing 10 items of 37 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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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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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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Roles of TP53 in determining therapeutic sensitivity, growth, cellular senescence, invasion and metastasis.

2016

TP53 is a critical tumor suppressor gene that regulates cell cycle progression, apoptosis, cellular senescence and many other properties critical for control of normal cellular growth and death. Due to the pleiotropic effects that TP53 has on gene expression and cellular physiology, mutations at this tumor suppressor gene result in diverse physiological effects. T53 mutations are frequently detected in numerous cancers. The expression of TP53 can be induced by various agents used to treat cancer patients such as chemotherapeutic drugs and ionizing radiation. Radiation will induce Ataxia telangiectasia mutated (ATM) and other kinases that results in the phosphorylation and activation of TP53…

0301 basic medicineCancer Researchendocrine system diseasesMetastasimedicine.disease_causeMetastasisAntineoplastic AgentInvasionNeoplasmsTP53Neoplasm Metastasisbcl-2-Associated X ProteinAza CompoundProto-Oncogene ProteinApoptosis Regulatory ProteinbiologyCell CyclemiRMicroRNACell cycleCell biologyNeoplasm MetastasiGene Expression Regulation NeoplasticNutlin-3 chemosensitivityMdm2Molecular MedicineHumanSignal TransductionCyclin-Dependent Kinase Inhibitor p21Tumor suppressor genemiRsAntineoplastic AgentsCellular senescenceTP53; miRs; MDM2; Nutlin-3 chemosensitivity; Cellular senescence ; Invasion; Metastasis03 medical and health sciencesBcl-2-associated X proteinGeneticMDM2Proto-Oncogene ProteinsmicroRNAGeneticsmedicineHumansNeoplasm InvasivenessneoplasmsMolecular BiologyCell ProliferationNeoplasm InvasiveneAza CompoundsOncomirBridged Bicyclo Compounds HeterocyclicMicroRNAs030104 developmental biologyTumor progressionbiology.proteinNeoplasmTumor Suppressor Protein p53CarcinogenesisApoptosis Regulatory Proteins
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RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1 and TP53 pathways and regulatory miRs as therapeutic targets in hepatocellular carcinoma

2019

Introduction: Hepatocellular carcinoma (HCC) is a significant problem globally because of viral infections and the increasing incidence of obesity and fatty liver disease. However, it is difficult to treat because its inherent genetic heterogeneity results in activation of numerous signaling pathways. Kinases have been targeted for decades with varying results, but the development of therapeutic resistance is a major challenge. Areas covered: The key roles of the RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1, TP53 microRNAs (miRs) as therapeutic targets are discussed and we suggests novel approaches for targeting miRs or their downstream targets to combat HCC. We performed literature searches using…

0301 basic medicineMAPK/ERK pathwayCarcinoma HepatocellularHepatocellular carcinmamedicine.medical_treatmentClinical BiochemistryAntineoplastic AgentsmTORC1signal transduction inhibitorsTargeted therapy03 medical and health sciences0302 clinical medicineDrug DiscoverymicroRNAmedicinePTENAnimalsHumanscancerMolecular Targeted TherapyTP53HCCRAS/RAF/MEK/ERKProtein kinase BPI3K/AKT/mTOR pathwaymiRNAPharmacologybiologybusiness.industryKinaseLiver NeoplasmsMirhepatocellular carcinomatargeted therapyGene Expression Regulation NeoplasticMicroRNAssignal transduction inhibitor030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisbiology.proteinCancer researchMolecular MedicinePI3K/PTEN/AKTbusinessSignal Transduction
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Biomarkers for vascular ageing in aorta tissues and blood samples.

2019

Abstract Objectives Functional and quantitative alterations and senescence of circulating and expanded endothelial progenitor cells (EPC), as well as systemic and tissue modifications of angiogenetic and inflammatory molecules, were evaluated for predicting age-related vessel wall remodeling, correlating them to intima media thickness (IMT) in the common carotid artery (CCA), a biomarker of early cardiovascular disease and aortic root dilation. Populations and methods A homogenous Caucasian population was included in the study, constituted by 160 healthy subjects (80 old subjects, mean age 72 ± 6.4, range 66–83 years; and 80 younger blood donors, mean age 26.2 ± 3.4, range 21–33 years), and…

0301 basic medicineMaleVascular Endothelial Growth Factor AAgingPhysiologySystemic inflammationBiochemistryCarotid Intima-Media Thickness0302 clinical medicineEndocrinologySA-β-Gal activityp21 and p16 genesMedicineTP53Receptor Notch1AortaEndothelial Progenitor CellsAged 80 and overeducation.field_of_studyChemotaxisInflammatory cytokinesmedicine.anatomical_structurecardiovascular systemBiomarker (medicine)Femalemedicine.symptomTP53 p21 and p16 genesSenescenceAdultEndotheliumInflammatory cytokineNotch and TLR4Carotid Artery CommonPopulationProinflammatory cytokine03 medical and health sciencesYoung AdultTP53 p21 and p16 genemedicine.arteryGeneticsHumansEPC cell populationeducationMolecular BiologyEPC cell populationsAgedAortabusiness.industryEndothelium age-related impairmentCell BiologyChemokine CXCL12Toll-Like Receptor 4EPC cell populations; Endothelium age-related impairment; Inflammatory cytokines; Notch and TLR4; SA-β-Gal activity; TP53 p21 and p16 genesSettore MED/23030104 developmental biologyIntima-media thicknessbusiness030217 neurology & neurosurgeryBiomarkersExperimental gerontology
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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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TP53 and p16INK4A, but not H-KI-Ras, are involved in tumorigenesis and progression of pleomorphic adenomas.

2006

The putative role of TP53 and p16INK4A tumor suppressor genes and Ras oncogenes in the development and progression of salivary gland neoplasias was studied in 28 cases of pleomorphic adenomas (PA), 4 cases of cystic adenocarcinomas, and 1 case of carcinoma ex-PA. Genetic and epigenetic alterations in the above genes were analyzed by Polymerase Chain Reaction/Single Strand Conformational Polymorphism (PCR/SSCP) and sequencing and by Methylation Specific-PCR (MS-PCR). Mutations in TP53 were found in 14% (4/28) of PAs and in 60% (3/5) of carcinomas. Mutations in H-Ras and K-Ras were identified in4%(1/28) and7% (2/28) of PAs, respectively. Only 20% (1/5) of carcinomas screened displayed mutatio…

AdenomaAdenomaGenotypePhysiologyClinical BiochemistryBiologymedicine.disease_causeMethylationEpigenesis GeneticProto-Oncogene Proteins p21(ras)GenotypemedicineCarcinomaHumansEpigeneticsTP53GeneCyclin-Dependent Kinase Inhibitor p16Base SequenceSingle-strand conformation polymorphismCell BiologyMethylationmedicine.diseaseMolecular biologyCell Transformation NeoplasticMutationDisease ProgressionTumor Suppressor Protein p53Carcinogenesis
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Analysis of TP53, Ki-Ras and P16INK4A promoter methylation as potential prognostic factors in patients with colorectal cancer

2007

AnalysisTP53 Ki-Ras P16INK4A colorectal cancer
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