Search results for "Oncogene"

showing 10 items of 1005 documents

TWIST and p-Akt immunoexpression in normal oral epithelium, oral dysplasia and in oral squamous cell carcinoma

2010

Objectives: The aim of this study was to evaluate the immunoexpression of TWIST and p-Akt proteins in oral leukoplakia (OL) and oral squamous cell carcinoma (OSCC), correlating their expressions with the histological features of the lesions. Study design: Immunohistochemical studies were carried out on 10 normal oral epithelium, 30 OL and 20 OSCC formalin-fixed, paraffin-embedded tissue samples. Immunoperoxidase reactions for TWIST and p-Akt proteins were applied on the specimens and the positivity of the reactions was calculated for 1000 epithelial cells. Results: Kruskal-Wallis and Dunn’s post tests revealed a significant difference in TWIST and p-Akt immunoexpression among normal oral mu…

MalePathologymedicine.medical_specialtyEpitheliumTwist transcription factormedicineHumansGeneral DentistryMouth neoplasmOral DysplasiaOral Medicine and PathologyImmunoperoxidasebusiness.industryTwist-Related Protein 1CancerMiddle Aged:CIENCIAS MÉDICAS [UNESCO]medicine.diseaseEpitheliumstomatognathic diseasesmedicine.anatomical_structureOtorhinolaryngologyDysplasiaUNESCO::CIENCIAS MÉDICASCarcinoma Squamous CellImmunohistochemistryFemaleMouth NeoplasmsResearch-ArticleSurgeryLeukoplakia OralbusinessProto-Oncogene Proteins c-aktMedicina Oral Patología Oral y Cirugia Bucal
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Tolerance-Inducing Dose of 3-Nitropropionic Acid Modulates bcl-2 and bax Balance in the Rat Brain: A Potential Mechanism of Chemical Preconditioning

2000

Many studies have reported ischemia protection using various preconditioning techniques, including single dose 3-nitropropionic acid (3-NPA), a mitochondrial toxin. However, the cellular signal transduction cascades resulting in ischemic tolerance and the mechanisms involved in neuronal survival in the tolerant state still remain unclear. The current study investigated the mRNA and protein expression of the antiapoptotic bcl-2 and the proapoptotic bax, two antagonistic members of the bcl-2 gene family, in response to a single dose of 3-NPA, to global cerebral ischemia–reperfusion, and to the combination of both 3-NPA-pretreatment and subsequent global cerebral ischemia–reperfusion. Brain h…

MalePathologymedicine.medical_specialtyIschemiaPharmacologyBiology030218 nuclear medicine & medical imaging03 medical and health sciences0302 clinical medicineBcl-2-associated X proteinDrug toleranceProto-Oncogene ProteinsGene expressionmedicineAnimalsRNA MessengerRats WistarIschemic Preconditioningbcl-2-Associated X ProteinMessenger RNABrainDrug ToleranceNitro Compoundsmedicine.diseasePathophysiologyRatsReal-time polymerase chain reactionProto-Oncogene Proteins c-bcl-2NeurologyIschemic Attack TransientApoptosisbiology.proteinNeurology (clinical)PropionatesCardiology and Cardiovascular Medicine030217 neurology & neurosurgeryJournal of Cerebral Blood Flow & Metabolism
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Biphasic dermatofibrosarcoma protuberans with a labyrinthine plexiform high‐grade fibrosarcomatous transformation

2013

Several variants of dermatofibrosarcoma protuberans, a low-grade superficial sarcoma, are well recognized. The most prognostically important is the fibrosarcomatous variant. We report a case of biphasic dermatofibrosarcoma protuberans in which the high-grade component exhibited a previously undescribed plexiform pattern. A clinicopathological study complemented with immunohistochemical, ultrastructural, reverse transcription polymerase chain reaction and fluorescence in situ hybridization analyses of this unique case. Histopathologically, a conventional low-grade dermatofibrosarcoma protuberans was admixed with intratumoral high-grade areas showing a striking labyrinthine plexiform pattern …

MalePathologymedicine.medical_specialtySkin NeoplasmsHistologyOncogene Proteins FusionFibrosarcomaCD34DermatologyBiologyPathology and Forensic MedicinemedicineDermatofibrosarcoma protuberansHumansIn Situ Hybridization FluorescencePDGFBmedicine.diagnostic_testDermatofibrosarcomaMiddle AgedPrognosismedicine.diseaseImmunohistochemistryCell Transformation NeoplasticCOL1A1/PDGFB Fusion GeneImmunohistochemistrySarcomaImmunostainingFluorescence in situ hybridizationJournal of Cutaneous Pathology
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Clinicopathological and Immunohistochemical Study of Oral Amalgam Pigmentation

2012

Amalgam tattoo, the most common exogenous oral pigmentation, can sometimes be confused with melanotic lesions, being then biopsied. We present the clinicopathological characteristics of 6 biopsied cases (5 females and 1 male) of oral amalgam pigmentation. The most common location was the gingival mucosa, followed by the buccal and palatal mucosa. Morphology and distribution (stromal, perivascular, perineural, endomysial) of pigmentation was variable; there was only 1 case with fibrous capsular reaction and likewise only a single case of granulomatous foreign body reaction. Morphological variability is conditioned by the timing and amount of the pigment deposit, which is often associated wit…

MalePathologymedicine.medical_specialtyStromal cellBiopsyGingivaAntigens Differentiation MyelomonocyticHLA-DR alpha-ChainsDental AmalgamMelanosisDiagnosis DifferentialPhagocytosisAntigens CDMetals HeavyBiopsymedicineHumansMast CellsPigmentation disorderGranulomabiologymedicine.diagnostic_testCD117business.industryForeign-Body ReactionMacrophagesAmalgam tattooMouth MucosaGeneral MedicineBuccal administrationMiddle Agedmedicine.diseaseMelanosisCorrosionProto-Oncogene Proteins c-kitstomatognathic diseasesGranulomabiology.proteinFemaleMetallothioneinMicroscopy PolarizationbusinessPigmentation DisordersActa Otorrinolaringologica (English Edition)
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Id2 leaves the chromatin of the E2F4-p130-controlled c-myc promoter during hepatocyte priming for liver regeneration

2006

The Id (inhibitor of DNA binding or inhibitor of differentiation) helix–loop–helix proteins are involved in the regulation of cell growth, differentiation and cancer. The fact that the molecular mechanisms of liver regeneration are not completely understood prompted us to study the fate of Id2 in proliferating liver. Id2 increases in liver regeneration after partial hepatectomy, following the early induction of its gene. Co-immunoprecipitation shows that Id2 forms a complex with E2F4, p130 and mSin3A in quiescent liver and all these components are present at the c-myc promoter as shown using ChIP (chromatin immunoprecipitation). Activation of c-myc during hepatocyte priming (G0–G1 transitio…

MalePriming (immunology)E2F4 Transcription FactorId2Cell cycleBiologyBiochemistryProto-Oncogene Proteins c-mycE2FmedicineAnimalsHistone deacetylaseRats WistarPromoter Regions GeneticE2FMolecular BiologyE2F4Inhibitor of Differentiation Protein 2Cell BiologyMolecular biologyChromatinLiver regenerationLiver RegenerationRatsSpecific Pathogen-Free OrganismsUp-RegulationChromatinC-mycmedicine.anatomical_structureGene Expression RegulationHepatocyteHepatocytesLiver regenerationHistone deacetylaseCarrier ProteinsChromatin immunoprecipitationResearch Article
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Cytotoxic activity of the novel small molecule AKT inhibitor SC66 in hepatocellular carcinoma cells

2014

Hepatocellular carcinoma (HCC) is characterized by limited response to current drug therapies. Here, we report that SC66, a novel AKT inhibitor, reduced cell viability in a dose- and time-dependent manner, inhibited colony formation and induced apoptosis in HCC cells. SC66 treatment led to a reduction in total and phospho-AKT levels. This was associated with alterations in cytoskeleton organization, a reduction in expression levels of E-cadherin, β-catenin and phospho-FAK, together with up-regulation of Snail protein levels. All these alterations were coupled with anoikis cell death induction. In addition, SC66 induced the production of reactive oxygen species (ROS) and DNA damage. Pre-trea…

MaleProgrammed cell deathCarcinoma HepatocellularCytoskeleton organizationPyridinesMice NudeApoptosisBiologyMice03 medical and health sciences0302 clinical medicineanoikisCell Line TumorAnimalsHumansAnoikisViability assayHCCProtein Kinase InhibitorsProtein kinase BPI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biologySC660303 health sciencesCyclohexanonesCell growthAKTLiver NeoplasmsXenograft Model Antitumor AssaysMolecular biology3. Good healthOncologyApoptosis030220 oncology & carcinogenesismTORCancer researchHCC AKT mTOR SC66 anoikisProto-Oncogene Proteins c-aktResearch Paper
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Nitric Oxide Mediates Natural Polyphenol-induced Bcl-2 Down-regulation and Activation of Cell Death in Metastatic B16 Melanoma

2007

Intravenous administration to mice of trans-pterostilbene (t-PTER; 3,5-dimethoxy-4'-hydroxystilbene) and quercetin (QUER; 3,3',4',5,6-pentahydroxyflavone), two structurally related and naturally occurring small polyphenols, inhibits metastatic growth of highly malignant B16 melanoma F10 (B16M-F10) cells. t-PTER and QUER inhibit bcl-2 expression in metastatic cells, which sensitizes them to vascular endothelium-induced cytotoxicity. However, the molecular mechanism(s) linking polyphenol signaling and bcl-2 expression are unknown. NO is a potential bioregulator of apoptosis with controversial effects on Bcl-2 regulation. Polyphenols may affect NO generation. Short-term exposure (60 min/day) t…

MaleProgrammed cell deathCeramideEndotheliumDown-RegulationBiologyNitric OxideBiochemistryMicechemistry.chemical_compoundPhenolsCell Line TumorCell AdhesionmedicineAnimalsRNA MessengerNeoplasm MetastasisCytotoxicityMelanomaMolecular BiologyNitritesFlavonoidsNitratesCell DeathReverse Transcriptase Polymerase Chain ReactionPolyphenolsHydrogen PeroxideCell BiologyGenes bcl-2Cell biologyMice Inbred C57BLEndothelial stem cellmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2Mitochondrial permeability transition porechemistryCell cultureApoptosisMitochondrial MembranesCancer researchEndothelium VascularJournal of Biological Chemistry
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Glutamine potentiates TNF-α-induced tumor cytotoxicity

2001

L-glutamine (Gln) sensitizes tumor cells to tumor necrosis factor (TNF)-alpha-induced cytotoxicity. The type and mechanism of cell death induced by TNF-alpha was studied in Ehrlich ascites tumor (EAT)-bearing mice fed a Gln-enriched diet (GED; where 30% of the total dietary nitrogen was from Gln). A high rate of Gln oxidation promotes a selective depletion of mitochondrial glutathione (mtGSH) content to approximately 58% of the level found in tumor mitochondria of mice fed a nutritionally complete elemental diet (standard diet, SD). The mechanism of mtGSH depletion involves a glutamate-induced inhibition of GSH transport from the cytosol into mitochondria. The increase in reactive oxygen in…

MaleProgrammed cell deathFree RadicalsCell SurvivalGlutamineApoptosisCytochrome c GroupMitochondrionBiologyBiochemistryMembrane PotentialsMiceNecrosischemistry.chemical_compoundAdenosine TriphosphateSuperoxidesPhysiology (medical)Tumor Cells CulturedAnimalsButhionine sulfoximineCaspase 3Tumor Necrosis Factor-alphaDrug SynergismHydrogen PeroxideGlutathioneGlutathioneMolecular biologyDietMitochondriaCell biologyOxygenGlutamineOxidative StressCytosolProto-Oncogene Proteins c-bcl-2chemistryApoptosisCaspasesReactive Oxygen SpeciesOxidation-ReductionCell DivisionIntracellularFree Radical Biology and Medicine
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2-Hydroxyoleate, a nontoxic membrane binding anticancer drug, induces glioma cell differentiation and autophagy

2012

Despite recent advances in the development of new cancer therapies, the treatment options for glioma remain limited, and the survival rate of patients has changed little over the past three decades. Here, we show that 2-hydroxyoleic acid (2OHOA) induces differentiation and autophagy of human glioma cells. Compared to the current reference drug for this condition, temozolomide (TMZ), 2OHOA combated glioma more efficiently and, unlike TMZ, tumor relapse was not observed following 2OHOA treatment. The novel mechanism of action of 2OHOA is associated with important changes in membrane-lipid composition, primarily a recovery of sphingomyelin (SM) levels, which is markedly low in glioma cells bef…

MaleProgrammed cell deathTime FactorsCell SurvivalMAP Kinase Signaling SystemCellular differentiationMice NudeAntineoplastic AgentsOleic AcidsBiologyglioma biomarkerfatty acidsMembrane LipidsMicePhosphatidylinositol 3-Kinases2-Hydroxyoleic AcidGliomaCell Line TumormedicineAutophagyTemozolomideAnimalsHumansPI3K/AKT/mTOR pathwayCell ProliferationMultidisciplinaryTemozolomideMicroscopy ConfocalDose-Response Relationship DrugCell growthCell MembraneRetinoblastoma proteinCell DifferentiationGliomaBiological Sciencesmedicine.diseaseXenograft Model Antitumor AssaysCell biologyDacarbazineProtein TransportCancer researchbiology.proteinras Proteinssphingomyelin synthaseProto-Oncogene Proteins c-aktcancer drug targetmedicine.drug
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Bcl-2 and Mn-SOD antisense oligodeoxynucleotides and a glutamine-enriched diet facilitate elimination of highly resistant B16 melanoma cells by tumor…

2005

Mitochondrial glutathione (mtGSH) depletion increases sensitivity of Bcl-2-overexpressing B16 melanoma (B16M)-F10 cells (high metastatic potential) to tumor necrosis factor-alpha (TNF-alpha)-induced oxidative stress and death in vitro. In vivo, mtGSH depletion in B16M-F10 cells was achieved by feeding mice (where the B16M-F10 grew as a solid tumor in the footpad) with an L-glutamine (L-Gln)-enriched diet, which promoted in the tumor cells an increase in glutaminase activity, accumulation of cytosolic L-glutamate, and competitive inhibition of GSH transport into mitochondria. L-Gln-adapted B16M-F10 cells, isolated using anti-Met-72 monoclonal antibodies and flow cytometry-coupled cell sortin…

MaleProgrammed cell deathgovernment.form_of_governmentGlutamineSOD2Antineoplastic AgentsSoft Tissue NeoplasmsMitochondrionBiologyBiochemistryGlutaminase activitySuperoxide dismutaseMiceAnimalsMolecular BiologyMelanomaAntisense therapySuperoxide DismutaseTumor Necrosis Factor-alphaCell BiologyGenetic TherapyOligonucleotides AntisenseMolecular biologyAnimal FeedCombined Modality TherapyGlutathioneMitochondriaMice Inbred C57BLDisease Models AnimalOxidative StressMitochondrial permeability transition poreProto-Oncogene Proteins c-bcl-2Drug Resistance Neoplasmgovernmentbiology.proteinTumor necrosis factor alphaNeoplasm TransplantationThe Journal of biological chemistry
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