Search results for " FGFR"

showing 10 items of 12 documents

Long Pentraxin 3-Mediated Fibroblast Growth Factor Trapping Impairs Fibrosarcoma Growth

2018

Fibrosarcomas are soft tissue mesenchymal tumors originating from transformed fibroblasts. Fibroblast growth factor-2 (FGF2) and its tyrosine-kinase receptors (FGFRs) play pivotal roles in fibrosarcoma onset and progression, FGF2 being actively produced by fibroblasts in all stages along their malignant transformation to the fibrosarcoma stage. The soluble pattern recognition receptor long pentraxin-3 (PTX3) is an extrinsic oncosuppressor whose expression is reduced in different tumor types, including soft tissue sarcomas, via hypermethylation of its gene promoter. PTX3 interacts with FGF2 and other FGF family members, thus acting as a multi-FGF antagonist able to inhibit FGF-dependent neov…

0301 basic medicineCancer ResearchFGF; FGF-trap; FGFR; fibrosarcoma; long pentraxin-3Fibroblast growth factorlcsh:RC254-282Malignant transformation03 medical and health sciences0302 clinical medicinemedicineFGFFibrosarcomaFibroblastReceptorneoplasmsOriginal ResearchFGF-trapintegumentary systemChemistryFGFRMesenchymal stem cellPTX3medicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologymedicine.anatomical_structurelong pentraxin-3OncologyFibroblast growth factor receptor030220 oncology & carcinogenesisCancer researchfibrosarcomaFrontiers in Oncology
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FGFR a promising druggable target in cancer: Molecular biology and new drugs.

2017

Abstract: Introduction: The Fibroblast Growth Factor Receptor (FGFR) family consists of Tyrosine Kinase Receptors (TKR) involved in several biological functions. Recently, alterations of FGFR have been reported to be important for progression and development of several cancers. In this setting, different studies are trying to evaluate the efficacy of different therapies targeting FGFR. Areas Covered: This review summarizes the current status of treatments targeting FGFR, focusing on the trials that are evaluating the FGFR profile as inclusion criteria: Multi-Target, Pan-FGFR Inhibitors and anti-FGF (Fibroblast Growth Factor)/FGFR Monoclonal Antibodies. Expert opinion: Most of the TKR share …

0301 basic medicineFibroblast Growth FactorDruggabilityFibroblast growth factorTyrosine-kinase inhibitorReceptor tyrosine kinase0302 clinical medicineNeoplasmsFGFR inhibitorsFGFMolecular Targeted TherapyCancerCancer; FGF; FGFR; FGFR inhibitors; Drug Resistance Neoplasm; Fibroblast Growth Factors; Gene Fusion; Humans; Molecular Targeted Therapy; Mutation; Neoplasms; Protein Kinase Inhibitors; Receptors Fibroblast Growth Factor; Signal Transduction; Hematology; Oncology; Geriatrics and GerontologybiologyFGFRHematologyFGFR inhibitorOncologyFibroblast growth factor receptor030220 oncology & carcinogenesisembryonic structuresSignal transductionbiological phenomena cell phenomena and immunityGene FusionHumanSignal Transductionmusculoskeletal diseasesanimal structuresmedicine.drug_classProtein Kinase Inhibitor03 medical and health sciencesmedicineHumansProtein Kinase InhibitorsCancer; FGF; FGFR; FGFR inhibitorsbusiness.industryCancermedicine.diseaseMolecular biologyReceptors Fibroblast Growth FactorFibroblast Growth Factors030104 developmental biologyDrug Resistance NeoplasmCancer cellMutationbiology.proteinNeoplasmHuman medicineGeriatrics and GerontologybusinessCritical reviews in oncology/hematology
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NEGR1 and FGFR2 cooperatively regulate cortical development and core behaviours related to autism disorders in mice.

2018

See Contreras and Hippenmeyer (doi:10.1093/brain/awy218) for a scientific commentary on this article. Autism spectrum disorders (ASDs) are complex conditions with diverse aetiologies. Szczurkowska et al. demonstrate that two ASD-related molecules – FGFR2 and Negr1 – physically interact to act on the same downstream pathway, and regulate cortical development and ASD-relevant behaviours in mice. Identifying common mechanisms in ASDs may reveal targets for pharmacological intervention.

0301 basic medicineMAPK/ERK pathwaygenetic structuresAutism Spectrum DisorderFGFR2 signalingFibroblast growth factorReceptor tyrosine kinaseMiceautism; development; cell adhesion; in utero electroporation; FGFR2 signaling0302 clinical medicineCell MovementCerebral CortexMice KnockoutbiologyBehavior AnimalKinaseCell adhesion moleculeCell biologyProtein TransportSignal Transductionmusculoskeletal diseasesMAP Kinase Signaling SystemCell Adhesion Molecules NeuronalDendritic SpinesNeurogenesisautismDown-Regulationbehavioral disciplines and activities03 medical and health sciencesmental disordersmedicineAnimalsHumansAutistic DisorderReceptor Fibroblast Growth Factor Type 2developmentProtein kinase BFibroblast growth factor receptor 2Cell Membranecell adhesionOriginal Articlesin utero electroporationmedicine.diseaseMice Inbred C57BLDisease Models Animal030104 developmental biologyHEK293 Cellsbiology.proteinAutismNeurology (clinical)030217 neurology & neurosurgeryBrain : a journal of neurology
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Nintedanib in NSCLC: evidence to date and place in therapy

2016

The treatment of advanced non-small cell lung cancer (NSCLC) is currently driven by the detection of targetable oncogenic drivers, i.e. epidermal growth factor receptor, echinoderm microtubule-associated protein-like 4–anaplastic lymphoma kinase, etc. Those patients who are wildtype for known and valuable oncogenes can receive standard chemotherapy as first-line treatment, with the possibility of adding bevacizumab. With regard to second-line treatment, nintedanib can improve the efficacy of docetaxel. Nintedanib is a tyrosine kinase inhibitor targeting three angiogenesis-related transmembrane receptors. The usefulness of nintedanib as an anticancer agent for NSCLC has been proved by both …

0301 basic medicineOncologymedicine.medical_specialtyBevacizumabPDGFRmedicine.drug_classmedicine.medical_treatmentReviewsPharmacologyNSCLClcsh:RC254-282Tyrosine-kinase inhibitorTargeted therapy03 medical and health scienceschemistry.chemical_compoundangiogenesisVEGFR0302 clinical medicineInternal medicinemedicinenintedanibangiogenesis; FGFR; nintedanib; NSCLC; PDGFR; targeted therapy; VEGFR; OncologyEpidermal growth factor receptorChemotherapybiologybusiness.industryFGFRangiogenesilcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenstargeted therapy030104 developmental biologyTolerabilitychemistryDocetaxelOncology030220 oncology & carcinogenesisbiology.proteinNintedanibbusinessmedicine.drug
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Agonist-induced formation of FGFR1 homodimers and signaling differ among members of the FGF family

2011

Fibroblast growth factor receptor 1 (FGFR1) is known to be activated by homodimerization in the presence of both the FGF agonist ligand and heparan sulfate glycosaminoglycan. FGFR1 homodimers in turn trigger a variety of downstream signaling cascades via autophosphorylation of tyrosine residues in the cytoplasmic domain of FGFR1. By means of Bioluminescence Energy Resonance Transfer (BRET) as a sign of FGFR1 homodimerization, we evaluated in HEK293T cells the effects of all known FGF agonist ligands on homodimer formation. A significant correlation between BRET(2) signaling and ERK1/2 phosphorylation was observed, leading to a further characterization of the binding and signaling properties…

AgonistMAPK/ERK pathwaymedicine.drug_classBiophysicsSettore BIO/11 - Biologia MolecolareBiologyLigandsFibroblast growth factorSettore BIO/09 - FisiologiaBiochemistrychemistry.chemical_compoundFluorescence Resonance Energy TransfermedicineHumansReceptor Fibroblast Growth Factor Type 1Molecular BiologyMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Fibroblast growth factor receptor 1HEK 293 cellsAutophosphorylationCell BiologyHeparan sulfateFibroblast growth factors FGFR1 Homodimerization BRET MAPKCell biologyFibroblast Growth Factorsstomatognathic diseasesHEK293 CellschemistrySettore BIO/14 - FarmacologiaPhosphorylationHeparitin SulfateProtein MultimerizationBiochemical and Biophysical Research Communications
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PDGFRβ and FGFR2 mediate endothelial cell differentiation capability of triple negative breast carcinoma cells

2014

Triple negative breast cancer (TNBC) is a very aggressive subgroup of breast carcinoma, still lacking specific markers for an effective targeted therapy and with a poorer prognosis compared to other breast cancer subtypes. In this study we investigated the possibility that TNBC cells contribute to the establishment of tumor vascular network by the process known as vasculogenic mimicry, through endothelial cell differentiation. Vascular-like functional properties of breast cancer cell lines were investigated in vitro by tube formation assay and in vivo by confocal microscopy, immunofluorescence or immunohistochemistry on frozen tumor sections. TNBCs express endothelial markers and acquire th…

Cancer ResearchPathologymedicine.medical_specialtyPDGFRmedicine.medical_treatmentTriple Negative Breast NeoplasmsMice SCIDBiologyEndothelial cell differentiationTargeted therapyReceptor Platelet-Derived Growth Factor betachemistry.chemical_compoundBreast cancerCell Line TumorGeneticsmedicineAnimalsHumansVasculogenic mimicryBreastRNA Small InterferingReceptor Fibroblast Growth Factor Type 2skin and connective tissue diseasesTriple-negative breast cancerResearch ArticlesNeovascularization PathologicFGFREndothelial CellsCell DifferentiationGeneral MedicineTriple Negative Breast Neoplasmsmedicine.diseaseImmunohistochemistryVascular endothelial growth factorOncologychemistryVasculogenic mimicryCancer researchMolecular MedicineTNBC; Vasculogenic mimicry; PDGFR; FGFRTriple-Negative Breast CarcinomaFemaleRNA InterferenceTNBC
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Design, synthesis and biological evaluation of new anticancer drugs: FGFR inhibitors

2021

Fibroblast growth factor receptors (FGFRs) constitute a family of tyrosine kinases receptors (RTKs) that exert pivotal physiological functions in human embryonic and adult tissues. Hyperactivated FGFR signaling drives tumorigenesis in multiple cancer types, including lung and brain cancers. Great effort has been laid on the development of new compounds that specifically target the FGFR axis. However, cancer cell- based and microenvironmental resistance mechanisms against FGFR inhibitors often arise and are currently poorly understood. Furthermore, FGFR-targeted therapy often presents different side effects, e due to the broad biological spectrum of the FGFR signaling axis as well as to its …

DesignhypoxiabrainglioblastomatransitionAnticancer drugs FGFR Drug design Ubiquitin Brain tumor Glioblastoma Lung cancer NSCLC SCLC Copper complexes Hypoxia activated drugs Metal drugsSettore BIO/11 - Biologia MolecolareSettore CHIM/08 - Chimica Farmaceuticalungmetal complexeFGFR1Settore CHIM/03 - Chimica Generale E InorganicacopperSettore BIO/10 - BiochimicaFGFR4Settore BIO/14 - Farmacologiacancersynthesi
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FGF-2/FGFR1 neurotrophic system expression level and its basal activation do not account for the age-dependent decline of precursor cell proliferatio…

2010

It is largely accepted that neurogenesis in the adult brain decreases with age and reduced levels of local neurotrophic support is speculated to be a contributing factor. Among neurotrophic factors involved on neurogenesis, we focused our attention on the neurotrophic system fibroblast growth factor-2 (FGF-2) and its receptor FGFR1, a potent modulator of precursor cell proliferation. In the present work, we aimed to analyse if potential age-dependent changes of the FGF-2/FGFR1 neurotrophic system may give account for the age-dependent decline of precursor cell proliferation in the neurogenic region of the subventricular zone (SVZ) in the rat brain. Using in situ hybridization and western bl…

MaleAgingmedicine.medical_specialtySubventricular zoneNeurogenesisReceptor expressionFGF-2Subventricular zoneFibroblast growth factorSettore BIO/09 - FisiologiaCerebral VentriclesFGF-2; FGFR1; Neurogenesis; Subventricular zone; Neuronal precursor cells; AgingGrowth factor receptorNeurotrophic factorsInternal medicinePrecursor cellmedicineAnimalsRNA MessengerReceptor Fibroblast Growth Factor Type 1PhosphorylationRats WistarMolecular BiologyCell ProliferationMitogen-Activated Protein Kinase 3biologyPhospholipase C gammaGeneral NeuroscienceNeurogenesisBrainNeuronal precursor cellRatsAdult Stem CellsFGFR1medicine.anatomical_structureEndocrinologyBromodeoxyuridineGene Expression Regulationbiology.proteinFibroblast Growth Factor 1NeurogenesiFibroblast Growth Factor 2Neurology (clinical)Developmental BiologyNeurotrophinBrain Research
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BCL-XL inhibition induces an FGFR4-mediated rescue response in colorectal cancer

2022

The heterogeneous therapy response observed in colorectal cancer is in part due to cancer stem cells (CSCs) that resist chemotherapeutic insults. The anti-apoptotic protein BCL-XL plays a critical role in protecting CSCs from cell death, where its inhibition with high doses of BH3 mimetics can induce apoptosis. Here, we screen a compound library for synergy with low-dose BCL-XL inhibitor A-1155463 to identify pathways that regulate sensitivity to BCL-XL inhibition and reveal that fibroblast growth factor receptor (FGFR)4 inhibition effectively sensitizes to A-1155463 both in vitro and in vivo. Mechanistically, we identify a rescue response that is activated upon BCL-XL inhibition and leads …

MaleBH3 mimeticsIndolesAxitinibColonDrug Evaluation Preclinicalbcl-X Proteincolorectal cancerMice SCIDGeneral Biochemistry Genetics and Molecular BiologyresistanceMice Inbred NODstem cellsCell Line TumorBCL-XLBCL-XL FGFR4 colorectal cancer apoptosis.AnimalsHumansReceptor Fibroblast Growth Factor Type 4BenzothiazolesAgedCell DeathDrug SynergismMiddle AgedIsoquinolinesOrganoidsNeoplastic Stem CellsFGFR4FemaleMCL-1Colorectal NeoplasmsCell reports
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Acute intermittent nicotine treatment induces fibroblast growth factor-2 in the subventricular zone of the adult rat brain and enhances neuronal prec…

2007

Abstract Over the past years, evidence has accumulated that stem cells are present in the adult brain, and generate neurons and/or glia from two active germinal zones: the subventricular zone (SVZ) of the lateral ventricles and the subgranular zone (SGZ) of the dentate gyrus of the hippocampus. This study shows that acute intermittent nicotine treatment significantly enhances neuronal precursor cell proliferation in the SVZ of adult rat brain, but not in the SGZ of the hippocampus, and pre-treatment with mecamylamine, a nonselective nAChR antagonist, blocks the enhanced precursor proliferation by nicotine. This effect is supported by up-regulation of fibroblast growth factor-2 (FGF-2) mRNA …

MaleNicotinemedicine.medical_specialtyBasic fibroblast growth factorSubventricular zoneNicotinic AntagonistsReceptors NicotinicBiologyFibroblast growth factorSettore BIO/09 - FisiologiaHippocampusSubgranular zonechemistry.chemical_compoundLateral VentriclesInternal medicinePrecursor cellmedicineAnimalsPyrrolesNicotinic AgonistsRNA MessengerReceptor Fibroblast Growth Factor Type 1Rats WistarCell ProliferationNeuronsNeuronal PlasticityStem CellsGeneral NeuroscienceFibroblast growth factor receptor 1Dentate gyrusNeurogenesisCell DifferentiationNerve RegenerationRatsUp-RegulationCell biologymedicine.anatomical_structureEndocrinologynervous systemchemistryneurogenesis FGF-2 FGFR-1 subventricular zone nicotineFibroblast Growth Factor 2Neuroscience
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