Search results for "ErbB"

showing 10 items of 298 documents

The role of targeted therapy for gastrointestinal tumors

2014

Abstract: Many targeted drugs have been studied to target the molecular pathways involved in the development of gastrointestinal cancers. Anti-VEGF, anti-EGFR agents, and recently also multi-kinase inhibitor regorafenib, have already been available for the treatment of metastatic colorectal cancer patients. To date, Her-2 positive, gastric cancer patients, are also treated with trastuzumab, while the multi-targeted inhibitor, sorafenib, represents the standard treatment for hepatocellular carcinoma patients. Finally, sunitinib and everolimus, have been approved for the treatment of the neuroendocrine gastroenteropancreatic tumors. Actually a great number of further drugs are under preclinic…

SorafenibOncologyVascular Endothelial Growth Factor Amedicine.medical_specialtyReceptor ErbB-2Hepatocellular carcinomaSettore MED/06 - Oncologia Medicamedicine.medical_treatmentAntineoplastic AgentsNeuroendocrine tumorsTargeted therapyTargeted therapychemistry.chemical_compoundNeuroendocrine tumorTrastuzumabInternal medicineRegorafenibmedicineHumansGastrointestinal tumorsMolecular Targeted TherapyProtein Kinase InhibitorsGastrointestinal NeoplasmsEverolimusHepatologySunitinibbusiness.industryColorectal cancer; Gastric cancer; Gastrointestinal tumors; Hepatocellular carcinoma; Neuroendocrine tumors; Targeted therapy; Hepatology; GastroenterologyGastrointestinal tumorGastroenterologyCancermedicine.diseaseColorectal cancerErbB ReceptorsReceptors Vascular Endothelial Growth FactorchemistryHuman medicineNeuroendocrine tumorsbusinessGastric cancermedicine.drug
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Regulation ofMUC1Expression in Human Mammary Cell Lines by the c-ErbB2 and Ras Signaling Pathways

2001

The MUC1 protein is a highly O-glycosylated transmembrane molecule that is expressed at the luminal surface of most glandular epithelial cells and is upregulated in carcinomas. Here, we report the effect of the activation of the c-ErbB2 --Ras pathway on the expression of the MUC1 gene in the nontumorigenic mammary cell lines MTSV1-7 and HB2 and in the malignant cell lines T47D and ZR75. Endogenous levels of MUC1 mRNA and protein in HB2 clones permanently overexpressing c-ErbB2 or V12-H-Ras were markedly reduced compared with levels in the parental cell lines. Furthermore, in transient transfection assays, the transcription of a CAT reporter construct driven by the MUC1 promoter was inhibite…

Transcription GeneticReceptor ErbB-2Recombinant Fusion ProteinsMutantDown-RegulationBreast NeoplasmsBiologyTransfectionCell LineWortmanninPhosphatidylinositol 3-Kinaseschemistry.chemical_compoundGenes ReporterTranscription (biology)Anti-apoptotic Ras signalling cascadeTumor Cells CulturedGeneticsHumansBreastPromoter Regions Geneticskin and connective tissue diseasesneoplasmsMolecular BiologyMUC1Phosphoinositide-3 Kinase InhibitorsOncogeneMucin-1Cell BiologyGeneral MedicineGenes erbB-2Molecular biologyTransmembrane proteinCell biologyAndrostadienesGenes rasGene Expression Regulationchemistryras ProteinsFemaleSignal transductionWortmanninSignal TransductionDNA and Cell Biology
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Epigenetic activation of a cryptic TBC1D16 transcript enhances melanoma progression by targeting EGFR

2015

Metastasis is respoMetastasis is responsible for most cancer-related deaths, and, among common tumor types, melanoma is one with great potential to metastasize. Here we study the contribution of epigenetic changes to the dissemination process by analyzing the changes that occur at the DNA methylation level between primary cancer cells and metastases. We found a hypomethylation event that reactivates a cryptic transcript of the Rab GTPase activating protein TBC1D16 (TBC1D16-47 kDa; referred to hereafter as TBC1D16-47KD) to be a characteristic feature of the metastatic cascade. This short isoform of TBC1D16 exacerbates melanoma growth and metastasis both in vitro and in vivo. By combining imm…

Transcriptional ActivationGTPase-activating proteinImmunoprecipitationMice NudeEditorials: Cell Cycle FeaturesBiologyBioinformaticsMethylationGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticMetastasisMetastasisEpigènesiMetàstasiCell Line TumormedicineAnimalsImmunoprecipitationProtein IsoformsRNA MessengerEpigeneticsNeoplasm MetastasisRNA Small InterferingPromoter Regions GeneticProteïnes supressores de tumorsProtein Kinase InhibitorsMelanomaMelanomaGTPase-Activating ProteinsGeneral MedicineMethylationDNA MethylationPrognosismedicine.diseaseTumor suppressor proteinErbB ReceptorsMolecular WeightTreatment Outcomerab GTP-Binding ProteinsDNA methylationDisease ProgressionCancer researchRabMetilacióProtein BindingSignal TransductionEpigenesisNature Medicine
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Interactions between cholinergic and fibroblast growth factor receptors in brain trophism and plasticity

2014

Acetylcholine, acting on both nicotinic receptors (nAChRs) and muscarinic receptors (mAChRs), plays a role in the regulation of synaptic plasticity, being involved in the regulation of cellular processes and cognitive functions, such as learning, memory and attention. Recently, G protein coupled receptors (GPCRs), including mAChRs, have been reported to transactivate tyrosine-kinase receptors (RTK), such as epidermal growth factor receptor (EGFR), and initiate their intracellular signaling. In this minireview we have first analysed the RTK transactivation mechanisms, involving cholinergic receptors, and thereafter the interplay between AChR and neurotrophic factor systems built up by FGF2 a…

Transcriptional Activationmedicine.medical_specialtyClass C GPCRG protein coupled receptorBiologyCholinergic AgonistsBiochemistrySynaptic plasticityTransactivationNicotinic receptorNeurotrophic factorsInternal medicinemedicineAnimalsHumansReceptors CholinergicProtein Interaction MapsReceptorMolecular BiologyG protein-coupled receptorTransactivationNeuronal PlasticityFibroblast growth factor receptor 1Muscarinic receptorBrainReceptor Protein-Tyrosine KinasesCell BiologyGeneral MedicineReceptors Fibroblast Growth FactorErbB ReceptorsEndocrinologyFGFR1Fibroblast growth factor receptorFGFR1; G protein coupled receptor; Muscarinic receptors; Nicotinic receptors; Receptor-receptor interaction; Synaptic plasticity; Transactivation; Tyrosine-kinase receptorsSignal transductionTyrosine-kinase receptorsNeuroscienceReceptor-receptor interactionSignal Transduction
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Endothelin-1-Mediated Drug Resistance in EGFR-Mutant Non-Small Cell Lung Carcinoma.

2020

Abstract Progression on therapy in non-small cell lung carcinoma (NSCLC) is often evaluated radiographically, however, image-based evaluation of said therapies may not distinguish disease progression due to intrinsic tumor drug resistance or inefficient tumor penetration of the drugs. Here we report that the inhibition of mutated EGFR promotes the secretion of a potent vasoconstrictor, endothelin-1 (EDN1), which continues to increase as the cells become resistant with a mesenchymal phenotype. As EDN1 and its receptor (EDNR) is linked to cancer progression, EDNR-antagonists have been evaluated in several clinical trials with disappointing results. These trials were based on a hypothesis that…

Vascular Endothelial Growth Factor ACancer ResearchLung NeoplasmsAmbrisentanOncology and CarcinogenesisDrug ResistanceBiological AvailabilityAntineoplastic AgentsDrug resistanceCell LineMiceErlotinib HydrochlorideGefitinibIn vivomedicineAnimalsHumansOncology & CarcinogenesisNon-Small-Cell LungProtein Kinase InhibitorsLungCancerTumor microenvironmentTumorEndothelin-1business.industryCarcinomaLung CancerCancerEvaluation of treatments and therapeutic interventionsGefitinibmedicine.diseaseEndothelin 1Xenograft Model Antitumor AssaysErbB ReceptorsOncologyVasoconstriction5.1 Pharmaceuticals6.1 PharmaceuticalsCancer cellMutationCancer researchNeoplasmDevelopment of treatments and therapeutic interventionsbusinessmedicine.drug
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Predicting efficacy and toxicity in the era of targeted therapy: focus on anti-EGFR and anti-VEGF molecules

2011

The treatment of solid malignancies includes various target drugs, such as monoclonal antibodies and tyrosine kinase inhibitors, which exert their effect alone or in combination with chemotherapy. The main part of these molecules have a target on proteins of EGFR and VEGF pathways. The particular toxicity profile and the financial impact, deriving from the application of these agents in cancer treatment, prompted a lot of researches to define predictive factors of their efficacy. Various biomarker were identified among the components of the targeted pathways. However just few studies allowed to identify specific factors to predict the toxicity of these drugs. In this review EGFR and VEGF-re…

Vascular Endothelial Growth Factor Amedicine.drug_classSettore MED/06 - Oncologia Medicamedicine.medical_treatmentClinical BiochemistryAngiogenesis InhibitorsAntineoplastic AgentsPharmacologyMonoclonal antibodyTargeted therapyAntineoplastic AgentNeoplasmsProtein-Tyrosine KinasemedicineHumansAngiogenesis Inhibitors; Antibodies Monoclonal; Antineoplastic Agents; Humans; Neoplasms; Protein-Tyrosine Kinases; Receptor Epidermal Growth Factor; Treatment Outcome; Vascular Endothelial Growth Factor ATarget therapyPharmacologyAnti vegfChemotherapybusiness.industryAntibodies MonoclonalProtein-Tyrosine KinasesErbB ReceptorsTreatment OutcomeToxicityCancer researchBiomarker (medicine)NeoplasmReceptor Epidermal Growth FactorbusinessTyrosine kinaseAngiogenesis InhibitorHuman
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The effects of α-secretase ADAM10 on the proteolysis of neuregulin-1

2009

Although ADAM10 is a major alpha-secretase involved in non-amyloidogenic processing of the amyloid precursor protein, several additional substrates have been identified, most of them in vitro. Thus, therapeutical approaches for the prevention of Alzheimer's disease by upregulation of this metalloproteinase may have severe side effects. In the present study, we examined whether the ErbB receptor ligand neuregulin-1, which is essential for myelination and other important neuronal functions, is cleaved by ADAM10. Studies with beta- and gamma-secretase inhibitors, as well as with the metalloproteinase inhibitor GM6001, revealed an inhibition of neuregulin-1 processing in human astroglioma cell …

biologyADAM10Cell BiologySheddaseBiochemistryDownregulation and upregulationErbBIn vivoAmyloid precursor proteinbiology.proteinCancer researchAstrogliomaNeuregulin 1Molecular BiologyFEBS Journal
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Cytotoxicity of the Urokinase-Plasminogen Activator Inhibitor Carbamimidothioic Acid (4-Boronophenyl) Methyl Ester Hydrobromide (BC-11) on Triple-Neg…

2015

BC-11 is an easily synthesized simple thiouronium-substituted phenylboronic acid, which has been shown to be cytotoxic on triple negative MDA-MB231 breast cancer cells by inducing a perturbation of cell cycle when administered at a concentration equal to its ED50 at 72 h (117 μM). Exposure of cells to BC-11, either pre-absorbed with a soluble preparation of the N-terminal fragment of urokinase-plasminogen activator (uPa), or in co-treatment with two different EGFR inhibitors, indicated that: (i) BC-11 acts via binding to the N-terminus of the enzyme where uPa- and EGF receptor-recognizing sites are present, thereby abrogating the growth-sustaining effect resulting from receptor binding

boronic acidPharmaceutical ScienceGene ExpressionApoptosisAnalytical ChemistryDrug DiscoveryCytotoxic T cellSettore BIO/06 - Anatomia Comparata E CitologiaCytotoxicityEGFR inhibitorschemistry.chemical_classificationCell CycleDrug SynergismCell cycleBoronic AcidsMitochondriaErbB ReceptorsBiochemistryChemistry (miscellaneous)Molecular MedicinecytotoxicityFemaleQD0241Antineoplastic AgentsArticlelcsh:QD241-441plasminogen activator inhibitorbreast cancerlcsh:Organic chemistryCell Line TumorHumansPhysical and Theoretical ChemistryMammary Glands HumanCell ProliferationQD0415Reactive oxygen speciesHydrobromideOrganic ChemistryEpithelial CellsBC-11Molecular biologyUrokinase-Type Plasminogen ActivatorPlasminogen InactivatorsEnzymechemistryApoptosisQuinazolinesMDA-MB231 cellsReactive Oxygen Speciesboronic acid; BC-11; plasminogen activator inhibitor; breast cancer; cytotoxicity; MDA-MB231 cellsMolecules
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High expression of progesterone receptor may be an adverse prognostic factor in oestrogen receptor-negative/progesterone receptor-positive breast can…

2021

Oestrogen receptor (ER)-negative (–) progesterone receptor (PgR)-positive (+) is the least common combination of steroid receptor expression observed in breast cancer. There are many controversies regarding the actual existence of ER–/PgR+ phenotype. In the current study, we aimed to perform comprehensive immunohistochemical re-evaluation of ER–/PgR+ breast cancers from multiple institutions. A total of 135 cases of ER–/PgR+ breast cancer were collected from 11 institutions from the period 2006–2020 and subsequently stained with three clinically validated anti-ER antibody clones: SP1 (Roche), 1D5 (Dako), and EP1 (Dako), and two anti-PgR antibody clones: 636 (Dako), and 1E2 (Roche). Clinicop…

breast cancerReceptors EstrogenOestrogen receptorReceptor ErbB-2immunohistochemistryHumansBreast NeoplasmsFemaleprognosisReceptors Progesteroneprogesterone receptorPathology and Forensic MedicinePathology
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STAT5b is a key effector of NRG-1/ERBB4-mediated myocardial growth

2023

The growth factor Neuregulin-1 (NRG-1) regulates myocardial growth and is currently under clinical investigation as a treatment for heart failure. Here, we demonstrate in several in vitro and in vivo models that STAT5b mediates NRG-1/EBBB4-stimulated cardiomyocyte growth. Genetic and chemical disruption of the NRG-1/ERBB4 pathway reduces STAT5b activation and transcription of STAT5b target genes Igf1, Myc, and Cdkn1a in murine cardiomyocytes. Loss of Stat5b also ablates NRG-1-induced cardiomyocyte hypertrophy. Dynamin-2 is shown to control the cell surface localization of ERBB4 and chemical inhibition of Dynamin-2 downregulates STAT5b activation and cardiomyocyte hypertrophy. In zebrafish e…

cardiomyocyte hypertrophyNRG-1–ErbB pathwaygeenitsydäncardiomyocyte hyperplasiadynaminkasvutekijätsydänlihassairaudetsydänlihassoluthypertrofinen kardiomyopatiasignal transduceractivator of transcriptionsolufysiologia
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