Search results for "TYROSINE KINASE"

showing 10 items of 362 documents

Antagonistic feedback loops involving Rau and Sprouty in the Drosophila eye control neuronal and glial differentiation.

2013

During development, differentiation is often initiated by the activation of different receptor tyrosine kinases (RTKs), which results in the tightly regulated activation of cytoplasmic signaling cascades. In the differentiation of neurons and glia in the developing Drosophila eye, we found that the proper intensity of RTK signaling downstream of fibroblast growth factor receptor (FGFR) or epidermal growth factor receptor required two mutually antagonistic feedback loops. We identified a positive feedback loop mediated by the Ras association (RA) domain-containing protein Rau that sustained Ras activity and counteracted the negative feedback loop mediated by Sprouty. Rau has two RA domains t…

Receptors SteroidGTP'Blotting WesternIn situ hybridizationEyeBiochemistryReceptor tyrosine kinaseMicroscopy Electron TransmissionAnimalsDrosophila ProteinsEpidermal growth factor receptorReceptorMolecular BiologyTranscription factorIn Situ HybridizationFeedback PhysiologicalbiologyIntracellular Signaling Peptides and ProteinsMembrane ProteinsReceptor Protein-Tyrosine KinasesCell DifferentiationCell BiologyAnatomyPhenotypeImmunohistochemistryCell biologyProtein Structure TertiaryDNA-Binding ProteinsEnzyme ActivationCOUP Transcription FactorsGene Expression RegulationFibroblast growth factor receptorbiology.proteinDrosophilaNeurogliaProtein BindingSignal TransductionScience signaling
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Adjuvant Imatinib in Patients with GIST Harboring Exon 9 KIT Mutations : Results from a Multi-institutional European Retrospective Study

2022

[Purpose] The effect of high-dose imatinib (800 mg/day) on survival in the adjuvant treatment of patients with resected KIT exon 9–mutated gastrointestinal stromal tumors (GIST) is not established. Here, the association of dose and other clinicopathologic variables with survival was evaluated in a large multi-institutional European cohort.

STRUCTURAL BASISEXPRESSIONOncologyCancer Researchmedicine.medical_specialtyGastrointestinal Stromal Tumors3122 CancersMedizinAntineoplastic Agentsexon 9Adjuvants ImmunologicInternal medicinemedicineHumansFAILURERetrospective StudiesRISKRECEPTORGiSTProportional hazards modelbusiness.industryGASTROINTESTINAL STROMAL TUMORSHazard ratioImatinibRetrospective cohort studyExonsAdjuvant treatmentConfidence intervalGENOTYPEProto-Oncogene Proteins c-kitOncologyChemotherapy AdjuvantMutationPropensity score matchingCohortImatinib MesylateNeoplasm Recurrence LocalTYROSINE KINASE INHIBITORbusinessRare cancers Radboud Institute for Health Sciences [Radboudumc 9]medicine.drugGIST
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Real Life Study of Lenvatinib Therapy for Hepatocellular Carcinoma: RELEVANT Study

2021

<b><i>Introduction:</i></b> In the REFLECT trial, lenvatinib was found to be noninferior compared to sorafenib in terms of overall survival. Here, we analyze the effects of lenvatinib in the real-life experience of several centers across the world and identify clinical factors that could be significantly associated with survival outcomes. <b><i>Methods:</i></b> The study population was derived from retrospectively collected data of HCC patients treated with lenvatinib. The overall cohort included western and eastern populations from 23 center in five countries. <b><i>Results:</i></b> We included 1,325 patients with HCC …

Second lineSettore MED/12 - GastroenterologiaOncologyHepatologyHepatocellular carcinomaLenvatinibNonalcoholic fatty liver diseaseTyrosine kinase inhibitors.ALBINonalcoholic steatohepatitiNeutrophils to lymphocyte ratioOutcome
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The nucleotide and partial amino acid sequences of rat fetuin. Identity with the natural tyrosine kinase inhibitor of the rat insulin receptor.

1992

Fetuins are among the major plasma proteins, yet their biological role has remained elusive. Here we report the molecular cloning of rat fetuin and the sequence analysis of a full-length clone, RF619 of 1456 bp with an open reading frame of 1056 bp encoding 352 amino acid residues. The coding part of RF619 was identical with the cDNA sequence of the natural inhibitor of the insulin receptor tyrosine kinase from rat (pp63) except for four substitutions and a single base insertion causing divergence of the predicted protein sequences. Partial amino acid sequences of rat plasma fetuin were in agreement with the predictions based on the RF619 cDNA. Purified rat fetuin inhibited the insulin rece…

Sequence analysisMolecular Sequence DataBiochemistryTropomyosin receptor kinase CReceptor tyrosine kinaseSubstrate SpecificityComplementary DNASequence Homology Nucleic AcidAnimalsAmino Acid SequencePhosphorylationchemistry.chemical_classificationbiologyBase SequenceDNAProtein-Tyrosine KinasesFetuinMolecular biologyReceptor InsulinAmino acidRatsInsulin receptorBiochemistrychemistryROR1biology.proteinalpha-FetoproteinsEuropean journal of biochemistry
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Cardiovascular Damage Induced by Anti-VEGF Therapy

2018

Vascular endothelial growth factor (VEGF) plays an important role in maintaining the regular homeostasis of vascular walls. VEGF binds its receptor (VEGFR) promoting the regular survival and function of endothelial cells. Anti-VEGF and anti-VEGFR drugs inhibit the action of VEGF and VEGFR. These drugs can cause cardiovascular toxic effects such as arterial hypertension, thromboembolism, myocardial ischemia and heart failure. The monoclonal antibody bevacizumab and tyrosine kinase inhibitors (sorafenib, sunitinib, pazopanib, regorafenib, axitinib, cabozantinib, ponatinib) are the main inhibitors of VEGF, VEGFR and other tyrosine kinases. In this chapter we will illustrate the cardiovascular …

SorafenibCabozantinibSunitinibbusiness.industryAxitinibVascular endothelial growth factorPazopanibchemistry.chemical_compoundchemistryRegorafenibmedicineCancer researchbusinessTyrosine kinasemedicine.drug
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BIBF 1120/ nintedanib : a new triple angiokinase inhibitor-directed therapy in patients with non-small cell lung cancer.

2013

Abstract: Introduction: Several new targeted agents with anti-angiogenic properties have been developed recently, including vandetanib, sunitinib, sorafenib, bevacizumab and others. Tumor development, progression, metastasis are strongly linked to angiogenesis. Targeted agents like bevacizumab, a monoclonal antibody which targets VEGF, have been fully developed in several solid tumors. These new agents strongly advocate that targeting angiogenesis is one of the best approaches for cancer therapy. Areas covered: Those agents that target additional pro-angiogenic intracellular signaling pathways beyond VEGF signaling have also the potential to contribute to anticancer therapies. The authors p…

SorafenibIndolesLung NeoplasmsBevacizumabSettore MED/06 - Oncologia MedicaAngiogenesis InhibitorsPharmacologyVandetanibMetastasischemistry.chemical_compoundCarcinoma Non-Small-Cell LungmedicineAnimalsHumansPharmacology (medical)Lung cancerProtein Kinase InhibitorsPharmacologyNeovascularization Pathologicbusiness.industrySunitinibPharmacology. Therapyanti-angiogenesis BIBF 1120 nintedanib non-small cell lung cancer vascular endothelial growth factorGeneral MedicineProtein-Tyrosine Kinasesmedicine.diseaseVascular endothelial growth factorchemistryCancer researchNintedanibbusinessmedicine.drugExpert opinion on investigational drugs
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Show me your signaling– and I’ll tell you who you are

2009

See Article, pages 725–733Cancer research and therapy have come a long way:the field started out in search of a ‘‘magic bullet” accord-ing to Paul Ehrlich’s theory, and was hoping to identifya target which was pivotal to signaling survival in trans-formed cells. Indeed, certain diseases with monocausalmutations were identified, and targeting of the muta-tional products has helped in the design of treatmentstrategies. In chronic myeloid leukemia (CML), the con-stitutive activation of the tyrosine kinase BCR-ABL ispathognomonic [1], and multiple BCR-ABL kinaseinhibitors (e.g. imatinib mesylate, dasatinib, nilotinib)have been developed and successfully used in the treat-ment of CML offering near-…

SorafenibMAPK/ERK pathwayHepatologybusiness.industryPharmacologyDasatinibImatinib mesylateNilotinibmedicineCancer researchErlotinibbusinessTyrosine kinasePI3K/AKT/mTOR pathwaymedicine.drugJournal of Hepatology
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Conquests and perspectives of cardio-oncology in the field of tumor angiogenesis-targeting tyrosine kinase inhibitor-based therapy

2015

Abstract: Introduction: Angiogenesis is fundamental for tumor development and progression. Hence, anti-angiogenic drugs have been developed to target VEGF and its receptors (VEGFRs). Several tyrosine kinase inhibitors (TKIs) have been developed over the years and others are still under investigation, each anti-VEGFR TKI showing a different cardiotoxic profile. Knowledge of the cardiac side-effects of each drug and the magnitude of their expression and frequency can lead to a specific approach. Areas covered: This work reviews the mechanism of action of anti-VEGFR TKIs and the pathophysiological mechanisms leading to cardiotoxicity, followed by close examination of the most important drugs i…

SorafenibOncologymedicine.medical_specialtymedicine.drug_classSettore MED/06 - Oncologia MedicaAntineoplastic AgentsPharmacologyVandetanibModels BiologicalTyrosine-kinase inhibitorPazopanibchemistry.chemical_compoundInternal medicineRegorafenibNeoplasmsmedicineHumansPharmacology (medical)Molecular Targeted TherapyProtein Kinase Inhibitorstyrosine kinase inhibitor cardiac toxicityNeovascularization PathologicSunitinibbusiness.industryPharmacology. TherapyCancerHeartGeneral MedicineDrugs InvestigationalProtein-Tyrosine Kinasesmedicine.diseaseAxitinibReceptors Vascular Endothelial Growth FactorchemistryCardiovascular Diseasesbusinessmedicine.drug
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Antineoplastic Drug-Induced Cardiotoxicity: A Redox Perspective

2018

Antineoplastic drugs can be associated with several side effects, including cardiovascular toxicity (CTX). Biochemical studies have identified multiple mechanisms of CTX. Chemoterapeutic agents can alter redox homeostasis by increasing the production of reactive oxygen species (ROS) and reactive nitrogen species RNS. Cellular sources of ROS/RNS are cardiomyocytes, endothelial cells, stromal and inflammatory cells in the heart. Mitochondria, peroxisomes and other subcellular components are central hubs that control redox homeostasis. Mitochondria are central targets for antineoplastic drug-induced CTX. Understanding the mechanisms of CTX is fundamental for effective cardioprotection, without…

Stromal cellPhysiologymedicine.medical_treatmentTyrosine kinase inhibitorChemotherapy; HER-2 inhibitors; Oxidative/nitrosative stress; Tyrosine kinase inhibitors; Vascular endothelial growth factorReviewOxidative phosphorylation030204 cardiovascular system & hematologyMitochondrionPharmacologyChemotherapy; HER-2 inhibitors; Oxidative/nitrosative stress; Tyrosine kinase inhibitors; Vascular endothelial growth factor; Physiology; Physiology (medical)chemotherapyHER-2 inhibitorlcsh:Physiology03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhysiology (medical)tyrosine kinase inhibitorsMedicinechemotherapy HER-2 inhibitors oxidative/nitrosative stress vascular endothelial growth factor tyrosine kinase inhibitorsReactive nitrogen specieschemistry.chemical_classificationCardioprotectionReactive oxygen speciesChemotherapyCardiotoxicitylcsh:QP1-981vascular endothelial growth factorbusiness.industryOxidative/nitrosative strechemistry030220 oncology & carcinogenesisbusinessHER-2 inhibitorsoxidative/nitrosative stress
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Interplay of three G‑quadruplex units in the KIT promoter

2019

The proto-oncogene KIT encodes for a tyrosine kinase receptor, which is a clinically validated target for treating gastrointestinal stromal tumors. The KIT promoter contains a G-rich domain within a relatively long sequence potentially able to form three adjacent G-quadruplex (G4) units, namely, K2, SP, and K1. These G4 domains have been studied mainly as single quadruplex units derived from short truncated sequences and are currently considered promising targets for anticancer drugs, alternatively to the encoded protein. Nevertheless, the information reported so far does not contemplate the interplay between those neighboring G4s in the context of the whole promoter, possibly thwarting dru…

Stromal cellbiologyChemistryGeneral ChemistryG-quadruplexBiochemistryMolecular biologyProto-Oncogene MasCatalysisReceptor tyrosine kinaseG‐Quadruplex Multiple G4 cancerG-QuadruplexesProto-Oncogene Proteins c-kitColloid and Surface ChemistrySettore CHIM/03 - Chimica Generale E Inorganicabiology.proteinHumansPromoter Regions GeneticGene
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