Search results for "oncogene"

showing 10 items of 1005 documents

Ganciclovir-induced apoptosis in HSV-1 thymidine kinase expressing cells: critical role of DNA breaks, Bcl-2 decline and caspase-9 activation.

2002

Although ganciclovir (GCV) is most often used in suicide anticancer gene therapy, the mechanism of GCV-induced cell killing and apoptosis is not fully understood. We analysed the mechanism of apoptosis triggered by GCV using a model system of CHO cells stably transfected with HSV-1 thymidine kinase (HSVtk). GCV-induced apoptosis is due to incorporation of the drug into DNA resulting in replication-dependent formation of DNA double-strand breaks and, at later stages, S and G2/M arrest. GCV-provoked DNA instability was likely to be responsible for the observed initial decline in Bcl-2 level and caspase-9/-3 activation. Further decline in the Bcl-2 level was due to cleavage of the protein by c…

Cancer ResearchTime FactorsvirusesPoly ADP ribose polymeraseApoptosisCytochrome c GroupCHO CellsHerpesvirus 1 HumanTransfectionThymidine KinaseCricetinaeGeneticsAnimalsfas ReceptorMolecular BiologyGanciclovirbiologyReverse Transcriptase Polymerase Chain ReactionCytochrome cCell CycleTransfectionSuicide geneFas receptorMolecular biologyCaspase 9Enzyme ActivationGene Expression Regulation NeoplasticCell killingProto-Oncogene Proteins c-bcl-2ApoptosisThymidine kinaseCaspasesbiology.proteinPoly(ADP-ribose) PolymerasesDNA DamageOncogene
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Partial restoration of pre-transformation levels of lysyl oxidase and transin mRNAs in phenotypic ras revertants.

1995

Neoplastic transformation mediated by ras oncogenes is associated with deregulated expression of genes encoding, for example, various proteases, lysyl oxidase, and smooth-muscle α-actin. To define the role of these genes in the initiation or maintenance of the ras-transformed state, we compared their steady-state mRNA levels in two different sets of preneoplastic fibroblast lines, ras-transformed clones, and phenotypic revertants derived from them. Compared with the preneoplastic fibroblasts, the ras-transformed derivatives exhibited elevated levels of cathepsin L (major excreted protein), transin (stromelysin I, matrix metalloproteinase–3), and collagenase I (matrix metalloproteinase–1) mR…

Cancer ResearchTranscription GeneticCathepsin LBlotting WesternGene ExpressionLysyl oxidaseCell LineCathepsin LProtein-Lysine 6-OxidaseProto-Oncogene Proteins c-mycDownregulation and upregulationEndopeptidasesmedicineAnimalsNeoplastic transformationCollagenasesRNA MessengerFibroblastMolecular BiologyGeneMessenger RNAbiologyMetalloendopeptidasesPhenotypeMolecular biologyCathepsinsNeoplasm ProteinsRatsCysteine Endopeptidasesmedicine.anatomical_structureCell Transformation NeoplasticGenes rasPhenotypebiology.proteinMatrix Metalloproteinase 3Matrix Metalloproteinase 1Precancerous ConditionsMolecular carcinogenesis
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MUC1 oncoprotein promotes refractoriness to chemotherapy in thyroid cancer cells.

2007

Abstract Overexpression of MUC1 oncoprotein is frequently observed in cancer and contributes to confer resistance to genotoxic agents. Papillary, follicular, and anaplastic thyroid carcinomas are the three forms of thyroid epithelial cancer. Anaplastic tumors are less differentiated and extremely aggressive, characterized by a poor prognosis. Little is known about the role of MUC1 in thyroid cancer. We recently showed that autocrine production of interleukin (IL)-4 and IL-10 controls thyroid cancer cell survival, growth, and resistance to chemotherapy through activation of Janus-activated kinase/signal transducers and activators of transcription (JAK/STAT) and phosphatidylinositide 3′-OH ki…

Cancer ResearchTranscription GeneticDrug ResistanceApoptosisSuppressor of Cytokine Signaling ProteinsnPhosphatidylinositol 3-KinasesAntibioticsMedicineRNA Small InterferingThyroid cancerTumorAntibiotics AntineoplasticThyroidAntineoplasticInterleukin-10Mitochondriamedicine.anatomical_structureOncologyTranscriptionSignal TransductionDown-RegulationSmall InterferingTransfectionCell LineThyroid carcinomaSuppressor of Cytokine Signaling 1 ProteinGeneticSettore MED/04 - PATOLOGIA GENERALEAntigens NeoplasmCell Line TumorHumansThyroid NeoplasmsAnaplastic thyroid cancerAntigensProtein kinase BPI3K/AKT/mTOR pathwayAntibiotics Antineoplastic; Antigens Neoplasm; Apoptosis; Cell Line Tumor; Down-Regulation; Doxorubicin; Drug Resistance Neoplasm; Humans; Interleukin-10; Interleukin-4; Mitochondria; Mucin-1; Mucins; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; RNA Small Interfering; Signal Transduction; Suppressor of Cytokine Signaling 1 Protein; Suppressor of Cytokine Signaling Proteins; Thyroid Neoplasms; Transcription Genetic; Transfection; Cancer Research; Oncologybusiness.industryMucin-1MucinsCancermedicine.diseaseDoxorubicinDrug Resistance NeoplasmCancer cellCancer researchNeoplasmRNAInterleukin-4businessProto-Oncogene Proteins c-aktCancer research
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Pharmacologic activation of p53 elicits Bax-dependent apoptosis in the absence of transcription

2003

AbstractRecent efforts to develop pharmacologic agents that restore function to mutant forms of p53 hold significant promise in cancer therapy. Here, we examine the effects of such pharmacologic activation of p53 function using a small molecule, PRIMA-1, and a model system employing a p53 protein fused to a mutant steroid binding domain of the murine estrogen receptor (p53ERtam) that renders it responsive only in the presence of 4-hydroxytamoxifen. In either case, p53 activation triggered apoptosis that was not inhibited by the presence of macromolecular synthesis inhibitors. This p53-induced, transcription-independent apoptosis is Bax dependent, proceeds in the absence of a nucleus, and in…

Cancer ResearchTranscription GeneticRecombinant Fusion ProteinsMutantEstrogen receptorApoptosis03 medical and health sciencesMice0302 clinical medicineBcl-2-associated X proteinProto-Oncogene ProteinsTumor Cells CulturedAnimalsHumansCloning MolecularReceptorCells Cultured030304 developmental biologybcl-2-Associated X ProteinCell NucleusProtein Synthesis Inhibitors0303 health sciencesAza CompoundsbiologyCytochrome cCytochromes cCell BiologyFibroblastsBridged Bicyclo Compounds Heterocyclic3. Good healthCell biologyTransport proteinMitochondriaProtein TransportTamoxifenProto-Oncogene Proteins c-bcl-2Receptors EstrogenOncologyApoptosis030220 oncology & carcinogenesisMutationbiology.proteinTumor Suppressor Protein p53Binding domainCancer Cell
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Epigenetic Alterations Upstream and Downstream of p53 Signaling in Colorectal Carcinoma

2021

Simple Summary Colorectal cancer (CRC) belongs to the most common cancer types. It is well known that half of all CRC possess missense mutations in the TP53 tumor suppressor gene. However, the entire signaling cascade upstream and downstream of the p53 protein may also contribute to CRC development, if relevant players in this signaling cascade lost their function. Besides p53 loss-of-function by mutations, epigenetic changes (DNA methylation, post translational modifications of histones, micro-RNAs) play a vital role in CRC development. In the present review, we concentrated on the epigenetic modifications related to the entire p53 signal transduction cascade upstream and downstream of p53…

Cancer ResearchTumor suppressor genetumor suppressorUpstream and downstream (transduction)Reviewmedicine.disease_causeoncogenemicroRNAmedicineEpigeneticsneoplasmsRC254-282acetylationbiologymicro-RNANeoplasms. Tumors. Oncology. Including cancer and carcinogensMethylationdigestive system diseasesHistoneOncologyDNA methylationCancer researchbiology.proteinmethylationCarcinogenesiscarcinogenesissignal transductionCancers
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hOA-DN30: a highly effective humanized single-arm MET antibody inducing remission of ‘MET-addicted’ cancers

2022

Abstract Background The tyrosine kinase receptor encoded by the MET oncogene is a major player in cancer. When MET is responsible for the onset and progression of the transformed phenotype (MET-addicted cancers), an efficient block of its oncogenic activation results in potent tumor growth inhibition. Methods Here we describe a molecular engineered MET antibody (hOA-DN30) and validate its pharmacological activity in MET-addicted cancer models in vitro and in vivo. Pharmacokinetics and safety profile in non-human primates have also been assessed. Results hOA-DN30 efficiently impaired MET activation and the intracellular signalling cascade by dose and time dependent removal of the receptor fr…

Cancer ResearchTumorCorrectionProto-Oncogene Proteins c-metCell LineTargeted therapyMiceAntibody; Gastric cancer; MET oncogene; Targeted therapy; Animals; Cell Line Tumor; Cell Proliferation; Humans; Mice; Signal Transduction; Proto-Oncogene Proteins c-met; Stomach NeoplasmsOncologyStomach NeoplasmsCell Line TumorMET oncogeneAnimalsHumansGastric cancerAntibodyCell ProliferationSignal TransductionJournal of Experimental & Clinical Cancer Research
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Analysis of Antiproliferative and Chemosensitizing Effects of Sunitinib on Human Esophagogastric Cancer Cells: Synergistic Interaction With Vandetani…

2009

The receptor tyrosine kinases (RTKs), epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor 1-3 (VEGFR1-3), are frequently expressed in gastric cancer and are putative therapeutic targets in this disease. We have investigated the anti-proliferative and chemosensitizing properties of the multitargeted small-molecule RTK inhibitors sunitinib and vandetanib in a panel of 4 human gastric and esophageal cancer cell lines. In the 1st instance, the expression of potential targets of these small-molecule inhibitors was examined by reverse transcriptase-polymerase chain reaction, western blotting, and flow cytometry. EGFR mRNA and protein was detected in all cases, …

Cancer ResearchUmbilical VeinsIndolesEsophageal NeoplasmsApoptosisVandetanibTyrosine-kinase inhibitorReceptor tyrosine kinasechemistry.chemical_compoundPiperidinesSunitinibMedicineDrug InteractionsEpidermal growth factor receptorPhosphorylationCells CulturedbiologySunitinibReverse Transcriptase Polymerase Chain ReactionDrug SynergismFlow CytometryErbB ReceptorsOncologyPhosphorylationDrug Therapy Combinationmedicine.drugSignal Transductionmedicine.medical_specialtymedicine.drug_classBlotting WesternAntineoplastic AgentsStomach NeoplasmsInternal medicineHumansPyrrolesPropidium iodideRNA MessengerProtein Kinase InhibitorsCell ProliferationVascular Endothelial Growth Factor Receptor-1business.industryCancermedicine.diseaseVascular Endothelial Growth Factor Receptor-3Vascular Endothelial Growth Factor Receptor-2EndocrinologychemistryCancer researchbiology.proteinQuinazolinesEndothelium VascularbusinessProto-Oncogene Proteins c-akt
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AKT-independent signaling downstream of oncogenic PIK3CA mutations in human cancer.

2009

SummaryDysregulation of the phosphatidylinositol 3-kinase (PI3K) signaling pathway occurs frequently in human cancer. PTEN tumor suppressor or PIK3CA oncogene mutations both direct PI3K-dependent tumorigenesis largely through activation of the AKT/PKB kinase. However, here we show through phosphoprotein profiling and functional genomic studies that many PIK3CA mutant cancer cell lines and human breast tumors exhibit only minimal AKT activation and a diminished reliance on AKT for anchorage-independent growth. Instead, these cells retain robust PDK1 activation and membrane localization and exhibit dependency on the PDK1 substrate SGK3. SGK3 undergoes PI3K- and PDK1-dependent activation in PI…

Cancer Researchanimal structuresCell SurvivalClass I Phosphatidylinositol 3-KinasesAKT1AKT2Breast NeoplasmsCELLCYCLEBiologyProtein Serine-Threonine Kinasesmedicine.disease_causeArticle03 medical and health sciencesPhosphatidylinositol 3-Kinases0302 clinical medicineCell Line TumorNeoplasmsmedicinePTENHumansProtein kinase BneoplasmsPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesGene Expression ProfilingPTEN PhosphohydrolasePyruvate Dehydrogenase Acetyl-Transferring KinaseCell Biology3. Good healthEnzyme ActivationOncology030220 oncology & carcinogenesisCancer cellMutationCancer researchbiology.proteinFemaleSignal transductionCarcinogenesisProto-Oncogene Proteins c-aktSignal TransductionCancer cell
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Immune escape of AKT overexpressing ovarian cancer cells

2012

Platinum-resistance is the most crucial problem for treatment of ovarian cancer. There is a clinical need for new treatment strategies which overcome platinum resistance. As survival is strongly influenced by immunological parameters, immunotherapeutic strategies appear promising. Therefore a better understanding of the interaction between ovarian tumour cells and cells of the immune system is a necessary prerequisite. In the present study we aimed to enlighten the interactions between platinum resistant and platinum sensitive ovarian cancer cells and natural-killer (NK)-cells. Modified FATAL assay was used for determining the killing efficiency of NK-cells for the parental A2780 cells and …

Cancer Researchendocrine system diseasesUbiquitin-Protein LigasesCellApoptosisBiologymedicine.disease_causeInhibitor of Apoptosis ProteinsImmune systemCell Line TumormedicineHumansPlatinumOvarian NeoplasmsCancerCell cyclemedicine.diseaseBaculoviral IAP Repeat-Containing 3 Proteinfemale genital diseases and pregnancy complicationsGene Expression Regulation NeoplasticKiller Cells Naturalmedicine.anatomical_structureOncologyDrug Resistance NeoplasmCell cultureApoptosisCancer researchFemaleOvarian cancerCarcinogenesisProto-Oncogene Proteins c-aktInternational Journal of Oncology
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Influence of segmental chromosome abnormalities on survival in children over the age of 12 months with unresectable localised peripheral neuroblastic…

2014

Background: The prognostic impact of segmental chromosome alterations (SCAs) in children older than 1 year, diagnosed with localised unresectable neuroblastoma (NB) without MYCN amplification enrolled in the European Unresectable Neuroblastoma (EUNB) protocol is still to be clarified, while, for other group of patients, the presence of SCAs is associated with poor prognosis. Methods: To understand the role of SCAs we performed multilocus/pangenomic analysis of 98 tumour samples from patients enrolled in the EUNB protocol. Results: Age at diagnosis was categorised into two groups using 18 months as the age cutoff. Significant difference in the presence of SCAs was seen in tumours of patients…

Cancer Researchmedicine.medical_specialtyPathologyMYCN AmplificationKaplan-Meier EstimateunresectableGastroenterologyDisease-Free Survivalsegmental chromosome alterationsNeuroblastomaneuroblastomaDDX1FISHaCGHOlder patientsPeripheral Nervous System NeoplasmsInternal medicineNeuroblastomaMYCNmedicineHumansMultiplex ligation-dependent probe amplificationGainChromosome AberrationsOncogene ProteinsComparative Genomic HybridizationN-Myc Proto-Oncogene Proteinbusiness.industrySignificant differenceGene AmplificationSegmental Chromosome abnormalitiesInfantNuclear ProteinsChromosomePrognosislocalisedmedicine.diseaseDoenças GenéticasMLPA3. Good healthPeripheralOncologyMycn amplificationClinical StudyHistopathologybusinessBritish Journal of Cancer
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