Search results for "Proto-oncogene"

showing 10 items of 770 documents

Understanding the clinical behavior of relapsed colon cancers with microsatellite instability relative to BRAF mutations

2019

Background Microsatellite instable/deficient mismatch repair (MSI/dMMR) metastatic colorectal cancers have been reported to have a poor prognosis. Frequent co-occurrence of MSI/dMMR and BRAFV600E complicates the association. Patients and methods Patients with resected stage III colon cancer (CC) from seven adjuvant studies with available data for disease recurrence and MMR and BRAFV600E status were analyzed. The primary end point was survival after recurrence (SAR). Associations of markers with SAR were analyzed using Cox proportional hazards models adjusted for age, gender, performance status, T stage, N stage, primary tumor location, grade, KRAS status, and timing of recurrence. Results A…

Proto-Oncogene Proteins B-rafdeficient mismatch repairrecurrenceBrain Neoplasmsbusiness.industryGastrointestinal tumorMicrosatellite instabilityHematologyPrognosismedicine.diseasedigestive system diseasesText miningcolon cancerOncologyNeoplastic Syndromes HereditaryColonic NeoplasmsmedicineCancer researchHumansmicrosatellite instabilityNeoplasm Recurrence LocalColorectal NeoplasmsbusinessAnnals of Oncology
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High frequency of BRAF V600E mutation in Iranian population ameloblastomas

2020

Background Ameloblastoma is a common locally invasive but slow-growing neoplasm of the jaws with an odontogenic origin. Association between BRAF V600E mutation and clinicopathologic features and behavior of ameloblastoma remains controversial. This study aimed to evaluate BRAF V600E gene mutation and expression of its related proteins with clinicopathologic parameters in conventional ameloblastoma. Material and Methods 50 Formalin-fixed paraffin-embedded blocks were included in this study. Immunohistochemistry was done using rabbit monoclonal BRAF V600E mutation-specific antibody VE1. Quantitative real-time polymerase chain reaction assay was used for evaluating of BRAF V600E mutation. Resu…

Proto-Oncogene Proteins B-rafendocrine system diseasesGene mutationIranlaw.inventionAmeloblastoma03 medical and health sciences0302 clinical medicinelawBiomarkers TumorMedicineNeoplasmHumansAmeloblastomaGeneral DentistryneoplasmsPolymerase chain reactionOral Medicine and Pathologybiologybusiness.industryResearch030206 dentistrymedicine.disease:CIENCIAS MÉDICAS [UNESCO]digestive system diseasesOtorhinolaryngologyMonoclonalMutation (genetic algorithm)MutationUNESCO::CIENCIAS MÉDICASCancer researchbiology.proteinImmunohistochemistrySurgeryAntibodyNeoplasm Recurrence Localbusiness
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Systematic review of BRAF/MEK inhibitors‐induced Severe Cutaneous Adverse Reactions (SCARs)

2020

Severe cutaneous adverse reactions (SCARs) [Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), drug rash with eosinophilia and systemic syndrome (DRESS), acute generalized exanthematous pustulosis (AGEP), and generalized bullous fixed eruption (GBFE)] are severe drug reactions that often require hospitalization and could be fatal. BRAF and MEK inhibitors (BRAF/MEKi) are a standard of care in patients with BRAF-mutated metastatic melanomas. These agents are administered until disease progression or unacceptable toxicity occurs. This review has focus on BRAF/MEKi-induced SCARs. A systematic search of the following terms: 'vemurafenib', 'cobimetinib', 'dabrafenib', 'trametinib',…

Proto-Oncogene Proteins B-rafmedicine.medical_specialtyDermatologyCicatrix030207 dermatology & venereal diseases03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineHumansVemurafenibRetrospective StudiesMitogen-Activated Protein Kinase KinasesTrametinibCobimetinibbusiness.industryBinimetinibDabrafenibAcute generalized exanthematous pustulosismedicine.diseaseDermatologyToxic epidermal necrolysisInfectious DiseasesAcute Generalized Exanthematous PustulosischemistryDrug Hypersensitivity SyndromeStevens-Johnson Syndrome030220 oncology & carcinogenesisbusinessmedicine.drugJournal of the European Academy of Dermatology and Venereology
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Piclamilast inhibits the pro-apoptotic and anti-proliferative responses of A549 cells exposed to H(2)O(2) via mechanisms involving AP-1 activation.

2012

Reactive oxygen species (ROS) are involved in the pathogenesis of many inflammatory diseases such as chronic obstructive pulmonary disease (COPD). They can alter the expression of genes involved in cellular damage by activating transcription factors, including the NF-κB and the activator protein 1 (AP-1). Phosphodiesterase type 4 (PDE4) inhibitors have anti-inflammatory and antioxidant effects, as described in in vivo and in vitro COPD models. This study analysed the effects of piclamilast, a selective PDE4 inhibitor, on modulating the global gene expression profile in A549 cells exposed to H(2)O(2).Changes in gene expression were analysed using high-density Affymetrix microarrays and valid…

Proto-Oncogene Proteins c-junPyridinesActivating transcription factorApoptosisBiologymedicine.disease_causeBiochemistryAntioxidantschemistry.chemical_compoundPulmonary Disease Chronic ObstructiveIn vivoAnnexinCell Line TumorGene expressionmedicineHumansRNA MessengerPhosphorylationCell ProliferationOligonucleotide Array Sequence AnalysisA549 cellGene Expression ProfilingNF-kappa BGeneral MedicineCell Cycle CheckpointsHydrogen PeroxideMolecular biologyTranscription Factor AP-1chemistryGene Expression RegulationAlveolar Epithelial CellsBenzamidesPhosphodiesterase 4 InhibitorsSignal transductionReactive Oxygen SpeciesPiclamilastOxidative stressSignal TransductionFree radical research
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Theileria parasites secrete a prolyl isomerase to maintain host leukocyte transformation

2015

Infectious agents develop intricate mechanisms to interact with host cell pathways and hijack their genetic and epigenetic machinery to change host cell phenotypic states. Among the Apicomplexa phylum of obligate intracellular parasites, which cause veterinary and human diseases, Theileria is the only genus that transforms its mammalian host cells. Theileria infection of bovine leukocytes induces proliferative and invasive phenotypes associated with activated signalling pathways, notably JNK and AP-1 (ref. 2). The transformed phenotypes are reversed by treatment with the theilericidal drug buparvaquone. We used comparative genomics to identify a homologue of the peptidyl-prolyl isomerase PI…

Proto-Oncogene Proteins c-jun[SDV]Life Sciences [q-bio]Drug ResistanceparasitesBiologyArticleCell LineHost-Parasite InteractionsmiR-155TheileriaTheileriaLeukocytesProlyl isomeraseAnimalsHumanscancerSecretionNIMA-Interacting Peptidylprolyl IsomeraseZebrafishComputingMilieux_MISCELLANEOUSPeptidylprolyl isomeraseSKP Cullin F-Box Protein LigasesMultidisciplinaryProtein StabilityGeneral CommentaryIntracellular parasiteUbiquitinationPeptidylprolyl Isomerasebiology.organism_classificationXenograft Model Antitumor AssaysMolecular biology3. Good healthCell biologyUbiquitin ligaseNIMA-Interacting Peptidylprolyl IsomeraseTranscription Factor AP-1Cell Transformation NeoplasticSchistosoma haematobiumPIN1biology.proteinMedicineCattleNaphthoquinonesSignal Transduction
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Establishing PNB-qPCR for quantifying minimal ctDNA concentrations during tumour resection.

2017

The analysis of blood plasma or serum as a non-invasive alternative to tissue biopsies is a much-pursued goal in cancer research. Various methods and approaches have been presented to determine a patient’s tumour status, chances of survival, and response to therapy from serum or plasma samples. We established PNB-qPCR (Pooled, Nested, WT-Blocking qPCR), a highly specific nested qPCR with various modifications to detect and quantify minute amounts of circulating tumour DNA (ctDNA) from very limited blood plasma samples. PNB-qPCR is a nested qPCR technique combining ARMS primers, blocking primers, LNA probes, and pooling of multiple first round products for sensitive quantification of the sev…

Proto-Oncogene Proteins p21(ras)NeoplasmsDNA Mutational AnalysisMutationBiomarkers TumorHumansDNA NeoplasmReal-Time Polymerase Chain ReactionSensitivity and SpecificityArticleCirculating Tumor DNAScientific reports
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Morphological, biochemical, and molecular biological characterization of a rat rhabdomyosarcoma cell line during differentiation induction in vitro.

1990

BA-HAN-1C is a clonal rat rhabdomyosarcoma cell line consisting of proliferating mononuclear tumor cells, some of which spontaneously fuse to form terminally differentiated postmitotic myotubelike giant cells. Exposure to retinoic acid resulted in an inhibition of proliferation and a marked increase in cellular differentiation. The number of myotubelike giant cells significantly increased, and about 30% of the mononuclear tumor cells exhibited morphological features of rhabdomyogenic differentiation which were not observed in the mononuclear cells of untreated cultures. Morphological differentiation was paralleled by an increase in total creatine kinase activity as a biochemical marker of d…

Proto-OncogenesCell divisionHealth Toxicology and MutagenesisCellular differentiationTretinoinBiologyCell LineTretinoinProto-OncogenesRhabdomyosarcomaTumor Cells CulturedmedicineAnimalsRhabdomyosarcomaPublic Health Environmental and Occupational HealthCell Differentiationmedicine.diseaseMolecular biologyIn vitroRatsGene Expression Regulation NeoplasticCell cultureRat RhabdomyosarcomaCell DivisionResearch Articlemedicine.drugEnvironmental Health Perspectives
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Simvastatin Increases the Ability of Roflumilast N-oxide to Inhibit Cigarette Smoke-Induced Epithelial to Mesenchymal Transition in Well-differentiat…

2014

Cigarette smoking contributes to epithelial-mesenchymal transition (EMT) in COPD small bronchi as part of the lung remodeling process. We recently observed that roflumilast N-oxide (RNO), the active metabolite of the PDE4 inhibitor roflumilast, prevents cigarette smoke-induced EMT in differentiated human bronchial epithelial cells. Further, statins were shown to protect renal and alveolar epithelial cells from EMT. To analyze how RNO and simvastatin (SIM) interact on CSE-induced EMT in well-differentiated human bronchial epithelial cells (WD-HBEC) from small bronchi in vitro. Methods: WD-HBEC were stimulated with CSE (2.5%). The mesenchymal markers vimentin, collagen type I and α-SMA, the e…

Pulmonary and Respiratory MedicineCyclopropanesSimvastatinEpithelial-Mesenchymal TransitionAminopyridinesSaludVimentinBronchiPharmacologyMedicineHumansEpithelial–mesenchymal transitionRoflumilastCells Culturedbeta CateninLungbiologybusiness.industryMesenchymal stem cellSmokingEpithelial Cellsrespiratory systemTabaquismoIn vitroBlotTabacomedicine.anatomical_structureSimvastatinBenzamidesbiology.proteinCancer researchPhosphodiesterase 4 InhibitorsHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessReactive Oxygen SpeciesProto-Oncogene Proteins c-aktmedicine.drugCOPD
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Regulation of endothelial nitric oxide synthase (eNOS) in myocardium subjected to cardioplegic arrest.

2009

BACKGROUND: Nitric oxide (NO) production by both coronary endothelial cells and cardiomyocytes is thought to play a significant role in myocardial pathophysiology following ischemia/reperfusion (I/R). METHODS: In thirteen pigs subjected to 1 hour cardioplegic arrest (CA) on CPB, left ventricular (LV) biopsies were collected prior to CPB (baseline), at 60 min CPA, at 15 and 30 min reperfusion on CPB, and at 120 min post CPB. LV specimens were immunocytochemically stained against phospho-eNOS Ser1177 , phospho-eNOS Thr495 , phosphorylated ERK1/2, and AKT/PKB. Four additional pigs without CA served as controls. Cardiomyocytes were quantitatively investigated using TV densitometry (gray units: …

Pulmonary and Respiratory MedicineMaleThreoninemedicine.medical_specialtyTime FactorsNitric Oxide Synthase Type IIISwineHeart VentriclesIschemiaEnos phosphorylationVentricular Function LeftNitric oxidechemistry.chemical_compoundEnosInternal medicinemedicineSerineAnimalsPhosphorylationProtein kinase BMitogen-Activated Protein Kinase 1Cardiopulmonary BypassMitogen-Activated Protein Kinase 3Endothelial nitric oxide synthasebiologybusiness.industryMyocardiummedicine.diseasebiology.organism_classificationImmunohistochemistryMyocardial ContractionPathophysiologyEnzyme ActivationEndocrinologychemistryModels AnimalCardiologyHeart Arrest InducedPhosphorylationSurgeryFemaleCardiology and Cardiovascular MedicinebusinessProto-Oncogene Proteins c-aktThe Thoracic and cardiovascular surgeon
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Rho protein inactivation induced apoptosis of cultured human endothelial cells.

2002

Small GTP-binding Rho GTPases regulate important signaling pathways in endothelial cells, but little is known about their role in endothelial cell apoptosis. Clostridial cytotoxins specifically inactivate GTPases by glucosylation [ Clostridium difficile toxin B-10463 (TcdB-10463), C. difficile toxin B-1470 (TcdB-1470)] or ADP ribosylation ( C. botulinum C3 toxin). Exposure of human umbilical cord vein endothelial cells (HUVEC) to TcdB-10463, which inhibits RhoA/Rac1/Cdc42, or to C3 toxin, which inhibits RhoA, -B, -C, resulted in apoptosis, whereas inactivation of Rac1/Cdc42 with TcdB-1470 was without effect, suggesting that Rho inhibition was responsible for endothelial apoptosis. Disruptio…

Pulmonary and Respiratory Medicinerac1 GTP-Binding Proteinrho GTP-Binding ProteinsProgrammed cell deathUmbilical VeinsEndotheliumPhysiologyBacterial ToxinsCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisBcl-2-associated X proteinBacterial ProteinsPhysiology (medical)Proto-Oncogene ProteinsmedicineCyclic AMPIn Situ Nick-End LabelingHumanscdc42 GTP-Binding ProteinCells Culturedbcl-2-Associated X ProteinAdenosine Diphosphate RibosebiologyCaspase 3Intracellular Signaling Peptides and ProteinsCell BiologyCaspase 9Cell biologyNeoplasm ProteinsEndothelial stem cellmedicine.anatomical_structureCdc42 GTP-Binding ProteinProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisCaspasesbiology.proteinMyeloid Cell Leukemia Sequence 1 ProteinEndothelium VascularSignal transductionCarrier ProteinsrhoA GTP-Binding ProteinBH3 Interacting Domain Death Agonist ProteinSignal TransductionAmerican journal of physiology. Lung cellular and molecular physiology
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