Search results for "TP53"

showing 10 items of 37 documents

Targeted next generation sequencing of breast implant-associated anaplastic large cell lymphoma reveals mutations in JAK/STAT signalling pathway gene…

2016

Oncologymedicine.medical_specialtysocs1030230 surgerymedicine.disease_causestat303 medical and health sciencesDNMT3A; SOCS1; STAT3; TP53; breast implant-associated anaplastic large-cell lymphoma; somatic mutations0302 clinical medicineInternal medicinemedicineAnaplastic lymphoma kinasebreast implant-associated anaplastic large-cell lymphomaSTAT3Anaplastic large-cell lymphomaMutationbiologySuppressor of cytokine signaling 1hematologyLarge cellJAK-STAT signaling pathwaybreast implantâ associated anaplastic large-cell lymphomatp53medicine.diseaseLymphomabreast implant-associated anaplastic large-cell lymphoma; dnmt3a; socs1; somatic mutations; stat3; tp53; hematology030220 oncology & carcinogenesisdnmt3aCancer researchbiology.proteinsomatic mutationsbreast implant–associated anaplastic large-cell lymphoma; DNMT3A; SOCS1; somatic mutations; STAT3; TP53; Hematology
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DNA ploidy and S-phase fraction, but not p53 or NM23-H1 expression, predict outcome in colorectal cancer patients. Result of a 5-year prospective stu…

2002

Purpose: The aim of this study was to determine TP53 and NM23-H1 immunoreactivity, DNA ploidy, and S-phase fraction (SPF) in a series of 160 patients undergoing resective surgery for primary operable colorectal cancer (CRC) and to establish whether these alterations have any clinical value in predicting CRC patients' prognosis. Methods: TP53 and NM23-H1 expressions were evaluated on paraffin-embedded tissue by immunohistochemistry and DNA-ploidy and SPF on frozen tissue by flow-cytometric analysis. Results: The median follow-up time in our study group was 71 months (range 34-115 months). P53 protein expression was associated with distal tumors (P < 0.05) and DNA aneuploid tumors (P < …

OncologyCancer Researchmedicine.medical_specialtyPathologyFlow-cytometric variableTime FactorsTumor suppressor geneColorectal cancerPrognosiSettore MED/06 - Oncologia MedicaColonRectumBiologyAdenocarcinomaDisease-Free SurvivalS PhasePredictive Value of TestsInternal medicinemedicineBiomarkers TumorHumansStage (cooking)Prospective cohort studyMonomeric GTP-Binding ProteinsNeoplasm StagingTP53 expressionHematologyPloidiesGeneral MedicineDNA NeoplasmCell cycleNM23 Nucleoside Diphosphate Kinasesmedicine.diseaseColorectal cancerAdenocarcinoma MucinousImmunohistochemistrySurvival Analysismedicine.anatomical_structureTreatment OutcomeOncologyNucleoside-Diphosphate KinaseImmunohistochemistryLymph NodesTumor Suppressor Protein p53Colorectal NeoplasmsCell DivisionTranscription FactorsJournal of cancer research and clinical oncology
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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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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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Molecular detection of TP53, Ki-Ras and p16INK4A promoter methylation in plasma of patients with colorectal cancer and its association with prognosis…

2006

BACKGROUND:Despite the improvement in detection and surgical therapy in the last years, the outcome of patients affected by colorectal carcinoma (CRC) remains limited by metastatic relapse. The aim of this study was to investigate the presence of free tumor DNA in the plasma of CRC patients in order to understand its possible prognostic role. PATIENTS AND METHODS: Ki-Ras, TP53 mutations and p16(INK4A) methylation status were prospectively evaluated in tumor tissues and plasma of 66 CRC patients. RESULTS: In 50 of the 66 primitive tumor cases (76%) at least one significant alteration was identified in Ki-Ras and/or TP53 and/or p16(INK4A) genes. Eighteen of the 50 patients presented the same …

MaleOncologymedicine.medical_specialtySettore MED/06 - Oncologia MedicaColorectal cancerColorectal carcinoma Free-cell DNA Ki-Ras TP53DiseasePolymerase Chain ReactionInternal medicinePromoter methylationHumansMedicineProspective StudiesPromoter Regions GeneticProspective cohort studyneoplasmsPolymorphism Single-Stranded ConformationalAgedNeoplasm StagingP16 geneUnivariate analysisbusiness.industryGenes p16DNA NeoplasmHematologyMethylationDNA MethylationGenes p53Prognosismedicine.diseaseGenes rasOncologyCell-free fetal DNAFemaleColorectal NeoplasmsbusinessAnnals of Oncology
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EPV139/#616 TP53 mutations differentially affect prognosis of endometrial cancer: an in-silico approach

2021

business.industryEndometrial cancerIn silicomedicineCancer researchTp53 mutationmedicine.diseaseAffect (psychology)businessE-Posters
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Distinct Mutational Profile of Lynch Syndrome Colorectal Cancers Diagnosed under Regular Colonoscopy Surveillance

2021

Regular colonoscopy even with short intervals does not prevent all colorectal cancers (CRC) in Lynch syndrome (LS). In the present study, we asked whether cancers detected under regular colonoscopy surveillance (incident cancers) are phenotypically different from cancers detected at first colonoscopy (prevalent cancers). We analyzed clinical, histological, immunological and mutational characteristics, including panel sequencing and high-throughput coding microsatellite (cMS) analysis, in 28 incident and 67 prevalent LS CRCs (n total = 95). Incident cancers presented with lower UICC and T stage compared to prevalent cancers (p &lt

OncologyColorectal cancerColonoscopybiomarkkeritHEREDITARYGUIDELINESTp53 mutationmedicine.disease_causeMolecular level0302 clinical medicineRISKincident cancercancer preventionmedicine.diagnostic_testRGeneral MedicineTUMORSLynch syndrome3. Good healthsyöpäsolutCARCINOMAS030220 oncology & carcinogenesisMedicineDNA mismatch repair030211 gastroenterology & hepatologyKRAScarcinogenesiskoloskopiamedicine.medical_specialtyDATABASEcolorectal cancersuolistosyövätmikrosatelliititArticle03 medical and health sciencescolonoscopy screeningInternal medicinemutational profilingmedicineLynchin oireyhtymäPathologicalpaksusuolisyöpäCancer preventionmismatch repair deficiencybusiness.industryMicrosatellite instabilitySCREENING INTERVAL3126 Surgery anesthesiology intensive care radiologymedicine.diseasedigestive system diseasesMSH2Lynch syndromeMSH23121 General medicine internal medicine and other clinical medicineT-stageCLINICAL MANAGEMENTmicrosatellite instabilitymutaatiotbusinessJournal of Clinical Medicine
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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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Primary glioblastomas with and without EGFR amplification: Relationship to genetic alterations and clinicopathological features

2009

Glioblastomas express a notable heterogeneity in both the histological and cell patterns with glial astrocytic differentiation. Primary glioblastoma, which is the most frequent presentation (90-95%), occurs mainly in older patients and arises de novo, without any clinical or histological evidence of a less malignant precursor lesion. EGFR amplification has been identified as a genetic hallmark of primary glioblastomas and occurs in 40-60% of cases. However, there exist primary glioblastomas without EGFR amplification/overexpression. The purpose of this study was to stabilize the association between cases with and without EGFR gene amplification with clinical and genetic parameters in 45 cas…

Pathologymedicine.medical_specialtyEGFR AmplificationCellGeneral MedicineBiologyTp53 mutationmedicine.diseasePathology and Forensic Medicinemedicine.anatomical_structureOlder patientsCancer researchmedicinebiology.proteinClinicopathological featuresMdm2EGFR Gene AmplificationNeurology (clinical)neoplasmsGlioblastomaNeuropathology
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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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