Search results for "oncogene"

showing 10 items of 1005 documents

Thiocarbamate-Linked Polysulfonate–Peptide Conjugates As Selective Hepatocyte Growth Factor Receptor Binders

2014

The capacity of many proteins to interact with natural or synthetic polyanions has been exploited for modulating their biological action. However, the polydispersity of these macromolecular polyanions as well as their poor specificity is a severe limitation to their use as drugs. An emerging trend in this field is the synthesis of homogeneous and well-defined polyanion–peptide conjugates, which act as bivalent ligands, with the peptide part bringing the selectivity of the scaffold. Alternately, this strategy can be used for improving the binding of short peptides to polyanion-binding protein targets. This work describes the design and first synthesis of homogeneous polysulfonate–peptide con…

DendrimersBiomedical EngineeringPharmaceutical ScienceBioengineeringPeptidemacromolecular substancesPlasma protein bindingArticleReceptor tyrosine kinaseSubstrate SpecificityStructure-Activity RelationshipThiocarbamatesmedicineHumansStructure–activity relationshipPharmacologychemistry.chemical_classificationDose-Response Relationship DrugMolecular StructurebiologyHepatocyte Growth FactorChemistryOrganic Chemistrytechnology industry and agricultureProto-Oncogene Proteins c-metProtein Structure TertiaryThiocarbamateBiochemistryHepatocyte Growth Factor ReceptorProto-Oncogene Proteins c-metbiology.proteinHepatocyte growth factorSulfonic AcidsPeptidesProtein BindingBiotechnologymedicine.drugBioconjugate Chemistry
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The effect of long context exposure on cued conditioning and c-fos expression in the rat forebrain

2004

The c-fos expression was used to study the neural substrates of the cued fear conditioning acquisition, preceded by a short exposure versus a long exposure to the conditioning context. A long-context exposure (either during the night or during the day) prior to conditioning, was associated with low freezing in the learning test. Differences in the c-fos expression of CA1, CA3, BL Amygdala, LS and BNST were found between the short- or long-context groups with a pre-exposure before cued conditioning. Ce Amygdala showed no differences in the c-fos expression labeling. We reported the hippocampal c-fos activation during the cued fear conditioning acquisition. Specifically, the CA1 activation co…

Diagnostic ImagingMaleHippocampusCell CountContext (language use)Amygdalac-FosGeneralization PsychologicalRats Sprague-DawleyBehavioral NeuroscienceProsencephalonConditioning PsychologicalmedicineAnimalsFear conditioningFreezing Reaction CatalepticAssociation (psychology)Cued speechAnalysis of VarianceBehavior AnimalbiologyFearImmunohistochemistryRatsmedicine.anatomical_structureAcoustic StimulationGene Expression Regulationnervous systembiology.proteinConditioningCuesPsychologyProto-Oncogene Proteins c-fosNeuroscienceBehavioural Brain Research
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Mast cells promote homeostasis by limiting endothelin-1-induced toxicity

2004

Endothelin-1 (ET-1) is a 21-amino-acid peptide, derived from vascular endothelial cells, with potent vasoconstrictor activity. ET-1 has been implicated in diverse physiological or pathological processes, including the vascular changes associated with sepsis. However, the factors that regulate ET-1-associated toxicity during bacterial infections, or in other settings, are not fully understood. Both the pathology associated with certain allergic and autoimmune disorders, and optimal host defence against bacterial and parasitic infections are mediated by mast cells. In vitro, mast cells can produce ET-1 (ref. 11), undergo ET-1-dependent and endothelin-A receptor (ET(A))-dependent activation, a…

DiarrheaProteasesDrug-Related Side Effects and Adverse ReactionsCell SurvivalPeritonitisBiologyPeptides CyclicCell DegranulationBody TemperatureMiceChymasesIn vivomedicineAnimalsHomeostasisMast CellsReceptorEgtazic AcidMice KnockoutMultidisciplinaryEndothelin-1Stem CellsBody WeightSerine EndopeptidasesEndogenous mediatorMast cellEndothelin 1In vitroCell biologyMice Inbred C57BLSurvival RateProto-Oncogene Proteins c-kitmedicine.anatomical_structureMutationImmunologyFemaleOligopeptidesInjections IntraperitonealHomeostasisNature
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Activation of TRPC6 calcium channels by diacylglycerol (DAG)-containing arachidonic acid: A comparative study with DAG-containing docosahexaenoic acid

2006

We synthesized a diacylglycerol (DAG)-containing arachidonic acid, i.e., 1-stearoyl-2-arachidonyl-sn-glycerol (SAG), and studied its implication in the modulation of canonical transient receptor potential sub-type 6 (TRPC6) channels in stably-transfected HEK-293 cells. SAG induced the influx of Ca(2+), and also of other bivalent cations like Ba(2+) and Sr(2+), in these cells. SAG-evoked Ca(2+) influx was not due to its metabolites as inhibitors of DAG-lipase (RHC80267) and DAG-kinase (R50922) failed to inhibit the response of the same. To emphasise that SAG exerts its action via its DAG configuration, but not due to the presence of stearic acid at sn-1 position, we synthesized 1-palmitoyl-2…

Docosahexaenoic AcidsBiologyBiochemistryTRPC6DiglyceridesMicechemistry.chemical_compoundTransient receptor potential channelMembrane Microdomainsparasitic diseasesTRPC6 Cation ChannelAnimalsCells CulturedTRPC Cation ChannelsDiacylglycerol kinaseDose-Response Relationship DrugVoltage-dependent calcium channelGeneral MedicineRhc80267src-Family KinaseschemistryBiochemistrySU6656BiophysicsCalciumlipids (amino acids peptides and proteins)Arachidonic acidProto-oncogene tyrosine-protein kinase SrcBiochimie
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Cardiotoxicity mechanisms of the combination of BRAF-inhibitors and MEK-inhibitors.

2018

Many new drugs have appeared in last years in the oncological treatment scenario. Each drug carries an important set of adverse events, not less, cardiovascular adverse events. This aspect is even more important considering the increasing use of combination therapies with two drugs, or three drugs as in some ongoing clinical trials. Besides it represents a growing problem for Cardiologists, that face it in every day clinical practice and that will face it probably more and more in the coming years. This work reviews the mechanism of action of BRAF-inhibitors and MEK-inhibitors used together, the pathophysiological mechanisms that lead to cardiovascular toxicity. Particularly, it focuses on …

DrugCardiovascular toxicityBRAF inhibitorProto-Oncogene Proteins B-rafmedicine.medical_specialtyCombination therapySettore MED/06 - Oncologia Medicamedia_common.quotation_subjectDecreased ejection fraction030204 cardiovascular system & hematologyCardiovascular System03 medical and health sciences0302 clinical medicineCardiovascular toxicityAntineoplastic Combined Chemotherapy ProtocolsMedicineHumansPharmacology (medical)Intensive care medicineAdverse effectBRAF inhibitor; Cardio-oncology; Cardiovascular toxicity; Decreased ejection fraction; Hypertension; MEK inhibitor; Pharmacology; Pharmacology (medical)MelanomaProtein Kinase Inhibitorsmedia_commonPharmacologyMitogen-Activated Protein Kinase KinasesCardiotoxicityMEK inhibitorClinical Trials as Topicbusiness.industryMEK inhibitorCancermedicine.diseaseCardiotoxicityClinical trialCardio-oncology030220 oncology & carcinogenesisHypertensionbusinessPharmacologytherapeutics
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Intracellular retention of ABL kinase inhibitors determines commitment to apoptosis in CML cells

2012

PLoS one 7(7), e40853 (2012). doi:10.1371/journal.pone.0040853

Drugs and DevicesDrug Research and DevelopmentTime Factorsmedicine.drug_classChronic Myeloid LeukemiaIntracellular Spacelcsh:MedicineApoptosisPharmacologyPiperazinesTyrosine-kinase inhibitorHematologic Cancers and Related DisordersCell Line TumorLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesLeukemiasmedicineHumansAnnexin A5Proto-Oncogene Proteins c-abllcsh:ScienceProtein Kinase InhibitorsMyeloproliferative DisordersMultidisciplinaryABLDose-Response Relationship DrugCaspase 3Chemistrylcsh:RBiological activityImatinibHematologyrespiratory tract diseasesDasatinibKineticsPyrimidinesImatinib mesylatePharmacodynamicsBenzamidesImatinib MesylateMedicineATP-Binding Cassette Transporterslcsh:QDrug Screening Assays AntitumorSignal transductionIntracellularResearch ArticleSignal Transductionmedicine.drug
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PED Mediates AKT-Dependent Chemoresistance in Human Breast Cancer Cells

2005

Abstract Killing of tumor cells by cytotoxic therapies, such as chemotherapy or gamma-irradiation, is predominantly mediated by the activation of apoptotic pathways. Refractoriness to anticancer therapy is often due to a failure in the apoptotic pathway. The mechanisms that control the balance between survival and cell death in cancer cells are still largely unknown. Tumor cells have been shown to evade death signals through an increase in the expression of antiapoptotic molecules or loss of proapoptotic factors. We aimed to study the involvement of PED, a molecule with a broad antiapoptotic action, in human breast cancer cell resistance to chemotherapeutic drugs–induced cell death. We show…

EXPRESSIONAdultCancer ResearchProgrammed cell deathmedicine.medical_treatmentINHIBITIONApoptosisBreast NeoplasmsProtein Serine-Threonine KinasesDNA AntisenseACTIVATIONBreast cancerTransduction GeneticCell Line TumorProto-Oncogene ProteinsComplementary DNAmedicineHumansCytotoxic T cellPROTEIN-KINASE-CProtein kinase BAgedNeoplasm StagingChemotherapybusiness.industryDEATHIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesIN-VITROCHEMOTHERAPYMiddle AgedPhosphoproteinsmedicine.diseasePED/PEA-15Up-RegulationEnzyme ActivationOncologyDrug Resistance NeoplasmApoptosisCancer cellImmunologyCancer researchFemalePTEN GENEApoptosis Regulatory ProteinsbusinessProto-Oncogene Proteins c-aktCancer Research
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Targeting BCL-2 family proteins to overcome drug resistance in non-small cell lung cancer.

2007

Cytotoxic chemotherapies are standard of care for patients suffering from advanced non-small cell lung cancer (NSCLC). However, objective responses are only achieved in 20% of cases and long-term survival is rarely observed. Clinically applied anticancer drugs exert at least some of their activities by inducing apoptosis. A critical step in apoptotic signal transduction is the permeabilization of the mitochondrial outer membrane (MOM), which is regulated by the BCL-2 family of proteins. Hence, therapeutic targeting of BCL-2 proteins is a promising approach to increase the drug-sensitivity of cancers. To this end we have assessed the impact of conditional expression of the proapoptotic multi…

ElectrophoresisCancer ResearchProgrammed cell deathLung NeoplasmsPaclitaxelmedicine.medical_treatmentImmunoblottingAntineoplastic AgentsApoptosisDrug resistanceBiologyPermeabilityPiperazinesTargeted therapyNitrophenolsCarcinoma Non-Small-Cell LungCell Line TumormedicineCytotoxic T cellHumansLung cancerEtoposideSulfonamidesBcl-2 familyBiphenyl CompoundsButylated Hydroxytoluenemedicine.diseaseFlow CytometryImmunohistochemistryMitochondriaNeoplasm ProteinsGene Expression Regulation Neoplasticbcl-2 Homologous Antagonist-Killer ProteinOncologyProto-Oncogene Proteins c-bcl-2ApoptosisDoxorubicinDrug Resistance NeoplasmImmunologyCancer researchMyeloid Cell Leukemia Sequence 1 ProteinSignal transductionSignal TransductionInternational journal of cancer
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Adverse events associated with encorafenib plus binimetinib in the COLUMBUS study: incidence, course and management.

2019

Abstract Background Dual inhibition of the mitogen-activated protein kinase pathway with BRAF/MEK inhibitor (BRAFi/MEKi) therapy is a standard treatment for BRAFV600-mutant metastatic melanoma and has historically been associated with grade III pyrexia or photosensitivity depending on the combination used. The objective of this study was to fully describe adverse events from the COLUMBUS study evaluating the most recent BRAF/MEK inhibitor combination encorafenib+binimetinib. Patients and methods Patients with locally advanced, unresectable or metastatic BRAFV600-mutant melanoma were randomised to receive encorafenib 450 mg once daily plus binimetinib 45 mg twice daily, encorafenib 300 mg on…

Encorafenib0301 basic medicineOncologyMaleCancer ResearchSkin NeoplasmsBinimetinib; Encorafenib; Melanoma; Safety; Vemurafenib;MedizinBinimetinibchemistry.chemical_compound0302 clinical medicineAntineoplastic Combined Chemotherapy Protocols1306 Cancer ResearchVemurafenibMelanomaFatigueeducation.field_of_studySulfonamidesMEK inhibitorMelanomaStandard treatmentIncidence10177 Dermatology ClinicBinimetinibNauseaMiddle AgedOncology030220 oncology & carcinogenesis2730 OncologyFemaleSafetyMitogen-Activated Protein Kinasesmedicine.drugProto-Oncogene Proteins B-rafmedicine.medical_specialtyVomitingPopulation610 Medicine & health03 medical and health sciencesInternal medicinemedicineHumanseducationAdverse effectProtein Kinase Inhibitorsbusiness.industrymedicine.diseaseDiscontinuation030104 developmental biologychemistryVemurafenibMutationBenzimidazolesCarbamatesbusinessEuropean journal of cancer (Oxford, England : 1990)
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Important role of Nfkb2 in the KrasG12D-driven carcinogenesis in the pancreas

2021

Abstract Background Oncogenic Kras initiates and drives carcinogenesis in the pancreas by complex signaling networks, including activation of the NFκB pathway. Although recent evidence has shown that oncogenic gains in Nfκb2 collaborate with Kras in the carcinogenesis, no data at the level of genetics for the contribution of Nfκb2 is available so far. Methods We used Nfkb2 knock-out mice to decipher the role of the gene in Kras-driven carcinogenesis in vivo. Results We show that the Nfkb2 gene is needed for cancer initiation and progression in KrasG12D-driven models and this requirement of Nfkb2 is mechanistically connected to proliferative pathways. In contrast, Nfκb2 is dispensable in agg…

Endocrinology Diabetes and Metabolismmedicine.disease_causelaw.invention03 medical and health sciences0302 clinical medicinelawPancreatic cancermedicineGeneHepatologyOncogenebusiness.industryGastroenterologyCancermedicine.diseasedigestive system diseasesddc:medicine.anatomical_structure030220 oncology & carcinogenesisCancer researchSuppressor030211 gastroenterology & hepatologyKRASCarcinogenesisbusinessPancreas
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