Search results for "GF"

showing 10 items of 838 documents

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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Coexpresión de NG2/GFAP tras la diferenciación en células transfectadas con las mutaciones de GFAP y en células procedentes de gliomas indiferenciados

2020

Resumen: Introducción: La enfermedad de Alexander es una enfermedad rara causada por mutaciones en el gen que codifica la proteína glial ácida fibrilar (GFAP). En un estudio previo hemos observado que la diferenciación de neuroesferas transfectadas con estas mutaciones genera un tipo celular que comparte la expresión de GFAP y NG2. Objetivos: Determinar el efecto de las mutaciones en marcadores moleculares en comparación con células de glioma diferenciados que expresan simultáneamente GFAP y NG2. Métodos: Se utilizaron muestras de glioblastoma humana (GLM) y neuroesferas procedentes de rata transfectadas con mutaciones de GFAP para el análisis de la expresión tras diferenciación de GFAP y N…

0301 basic medicineGFAPmacromolecular substancesGliomalcsh:RC346-42903 medical and health sciences030104 developmental biology0302 clinical medicinenervous systemCaspase-3Alexander diseaseNG2Neurology (clinical)030217 neurology & neurosurgerylcsh:Neurology. Diseases of the nervous systemNeurología
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Homozygous FIBP nonsense variant responsible of syndromic overgrowth, with overgrowth, macrocephaly, retinal coloboma and learning disabilities

2016

The acidic fibroblast growth factor (FGF) intracellular binding protein (FIBP) interacts directly with the fibroblast growth factor FGF1. Although FIBP is known to be implicated in the FGF signaling pathway, its precise function remains unclear. Gain-of-function variants in several FGF receptors (FGFRs) are implicated in a wide spectrum of growth disorders from achondroplasia to overgrowth syndromes. In a unique case from a consanguineous union presenting with overgrowth, macrocephaly, retinal coloboma, large thumbs, severe varicose veins and learning disabilities, exome sequencing identified a homozygous nonsense FIBP variant. The patient's fibroblasts exhibit FIBP cDNA degradation and an …

0301 basic medicineGeneticsmedia_common.quotation_subjectNonsenseMacrocephaly030105 genetics & heredityFGF1BiologyFibroblast growth factormedicine.diseasePhenotype03 medical and health sciences030104 developmental biologyFibroblast growth factor receptorGeneticsmedicinemedicine.symptomAchondroplasiaGenetics (clinical)Exome sequencingmedia_commonClinical Genetics
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Simultaneous Boron Ion‐Channel/Growth Factor Receptor Activation for Enhanced Vascularization

2018

[EN] Boron ion is essential in metabolism and its concentration is regulated by ion-channel NaBC1. NaBC1 mutations cause corneal dystrophies such as Harboyan syndrome. Here we propose a 3D molecular model for NaBC1 and show that simultaneous stimulation of NaBC1 and vascular growth factor receptors (VEGFR) promote angiogenesis in vitro and in vivo with ultra-low concentrations of VEGF. We show Human Umbilical Vein Endothelial Cells (HUVEC) organization into tubular structures indicative of vascularization potential. Enhanced cell sprouting was found only in the presence of VEGF and boron, effect abrogated after blocking NaBC1. We demonstrate that stimulated NaBC1 promotes angiogenesis via P…

0301 basic medicineIntegrinsVEGF receptorsBiomedical EngineeringEuropean Regional Development FundLibrary scienceBoron ionGeneral Biochemistry Genetics and Molecular BiologyBiomaterials03 medical and health sciencesNaBC10302 clinical medicineGrowth factor receptorPolitical scienceFibronectinbiologyEuropean researchVascularizationChick embryosVEGFEngineering and Physical Sciences030104 developmental biologyResearch councilFISICA APLICADA030220 oncology & carcinogenesisbiology.proteinCam assayAdvanced Biosystems
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Transforming growth factor β (CiTGF-β) gene expression is induced in the inflammatory reaction of Ciona intestinalis.

2016

Transforming growth factor (TGF-β) is a well-known component of a regulatory cytokines superfamily that has pleiotropic functions in a broad range of cell types and is involved, in vertebrates, in numerous physiological and pathological processes. In the current study, we report on Ciona intestinalis molecular characterisation and expression of a transforming growth factor β homologue (CiTGF-β). The gene organisation, phylogenetic tree and modelling supported the close relationship with the mammalian TGF suggesting that the C. intestinalis TGF-β gene shares a common ancestor in the chordate lineages. Functionally, real-time PCR analysis showed that CiTGF-β was transcriptionally upregulated …

0301 basic medicineLipopolysaccharidesCell typeHemocytesTGFbeta Ciona intestinalisCellular differentiationImmunologyMolecular Sequence DataSettore BIO/05 - ZoologiaBiology03 medical and health sciences0302 clinical medicineImmune systemTranscription (biology)Transforming Growth Factor betaGene expressionAnimalsCiona intestinalisAmino Acid SequenceCloning MolecularGenePhylogenyInflammationMammalsbiology.organism_classificationImmunity InnateCell biologyCiona intestinalisUp-Regulation030104 developmental biologyImmunologyPharynx030217 neurology & neurosurgeryDevelopmental BiologyTransforming growth factorDevelopmental and comparative immunology
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Investigating fibrosis and inflammation in an ex vivo NASH murine model.

2020

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease, characterized by excess fat accumulation (steatosis). Nonalcoholic steatohepatitis (NASH) develops in 15–20% of NAFLD patients and frequently progresses to liver fibrosis and cirrhosis. We aimed to develop an ex vivo model of inflammation and fibrosis in steatotic murine precision-cut liver slices (PCLS). NASH was induced in C57Bl/6 mice on an amylin and choline-deficient l-amino acid-defined (CDAA) diet. PCLS were prepared from steatohepatitic (sPCLS) and control (cPCLS) livers and cultured for 48 h with LPS, TGFβ1, or elafibranor. Additionally, C57Bl/6 mice were placed on CDAA diet for 12 wk to receive elafibranor…

0301 basic medicineLipopolysaccharidesLiver CirrhosisMalePhysiologyHEPATOCYTESLiver diseaseMice0302 clinical medicineChalconesFibrosisNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseaseCells CulturedINSULIN-RESISTANCEGastroenterologyElafibranorTGF-BETALiver030211 gastroenterology & hepatologyCHOLINE-DEFICIENT DIETEXPRESSIONmedicine.medical_specialtyEARLY-ONSETIn Vitro TechniquesCollagen Type IProinflammatory cytokineTransforming Growth Factor beta103 medical and health sciencesIn vivoPhysiology (medical)Internal medicinemedicineAnimalsHEPATIC STEATOSISFATTY LIVER-DISEASEInflammationPRECISION-CUT LIVERHepatologybusiness.industrymedicine.diseaseLipid MetabolismDietMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyPROLIFERATOR-ACTIVATED RECEPTORSSteatosisPropionatesbusinessTranscriptomeEx vivoAmerican journal of physiology. Gastrointestinal and liver physiology
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Pharmacokinetics of a sustained release formulation of PDGFβ-receptor directed carrier proteins to target the fibrotic liver

2018

Liver fibrogenesis is associated with excessive production of extracellular matrix by myofibroblasts that often leads to cirrhosis and consequently liver dysfunction and death. Novel protein-based antifibrotic drugs show high specificity and efficacy, but their use in the treatment of fibrosis causes a high burden for patients, since repetitive and long-term parenteral administration is required as most proteins and peptides are rapidly cleared from the circulation. Therefore, we developed biodegradable polymeric microspheres for the sustained release of proteinaceous drugs. We encapsulated the drug carrier pPB-HSA, which specifically binds to the PDGF beta R that is highly upregulated on a…

0301 basic medicineLiver CirrhosisMaleCirrhosisPolymersLiver fibrosisPharmaceutical Science02 engineering and technologyPharmacologyMULTIBLOCK-COPOLYMERReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesPharmacokineticsFibrosisIn vivomedicinein vitro in vivo correlationAnimalsControlled releaseFIBROSISBiodegradable polymeric microspheresDRUG-DELIVERYSerum AlbuminIN-VIVOMice KnockoutPOLYMERIC MICROSPHERESDrug CarriersINTERFERON-GAMMAChemistryProtein deliveryAlbuminPDGF beta-receptor targeted drug carrier021001 nanoscience & nanotechnologymedicine.diseaseControlled releaseIMPLANTSMicrospheresANTIFIBROTIC THERAPIESMice Inbred C57BLMICE030104 developmental biologyDelayed-Action PreparationsDrug delivery0210 nano-technologyDrug carrierGROWTH-FACTOR RECEPTOR
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Amphiregulin contained in NSCLC-exosomes induces osteoclast differentiation through the activation of EGFR pathway

2017

AbstractNon-small cell lung cancer (NSCLC) remains the leading cause of cancer-related deaths worldwide. The majority of patients are diagnosed in advanced disease stage. Bone metastasis is the most frequent complication in NSCLC resulting in osteolytic lesions. The perfect balance between bone-resorbing osteoclasts and bone-forming osteoblasts activity is lost in bone metastasis, inducing osteoclastogenesis. In NSCLC, the epidermal growth factor receptor (EGFR) pathway is constitutively activated. EGFR binds Amphiregulin (AREG) that is overexpressed in several cancers such as colon, breast and lung. Its levels in plasma of NSCLC patients correlate with poor prognosis and AREG was recently …

0301 basic medicineLung NeoplasmsCellular differentiationAmphiregulin exosomes NSCLC EGFROsteoclastsExosomes NSCLC AmphiregulinNSCLCExosomesMice0302 clinical medicineSettore BIO/13 - Biologia ApplicataCarcinoma Non-Small-Cell LungMedicineEpidermal growth factor receptorRNA Small InterferingMultidisciplinarybiologyQProteolytic enzymesRBone metastasisCell Differentiation3. Good healthErbB ReceptorsGene Expression Regulation Neoplasticmedicine.anatomical_structureRANKL030220 oncology & carcinogenesisMedicineEngineering sciences. TechnologySciencePrimary Cell CultureBone NeoplasmsAmphiregulinArticle03 medical and health sciencesAmphiregulinOsteoclastCell Line TumorAnimalsHumansbusiness.industryRANK LigandBiological Transportmedicine.diseaseMicrovesiclesCoculture Techniquesrespiratory tract diseases030104 developmental biologyRAW 264.7 CellsImmunologybiology.proteinCancer researchbusiness
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Profile of the Roche cobas® EGFR mutation test v2 for non-small cell lung cancer

2017

Abstract: Introduction: The discovery of driver mutations in non-small cell lung cancer (NSCLC) has led to the development of genome-based personalized medicine. Fifteen to 20% of adenocarcinomas harbor an epidermal growth factor receptor (EGFR) activating mutation associated with responses to EGFR tyrosine kinase inhibitors (TKIs). Individual laboratories' expertise and the availability of appropriate equipment are valuable assets in predictive molecular pathology, although the choice of methods should be determined by the nature of the samples to be tested and whether the detection of only well-characterized EGFR mutations or rather, of all detectable mutations, is required.Areas covered:…

0301 basic medicineLung NeoplasmsEGFRDNA Mutational Analysis2734Real-Time Polymerase Chain Reactionmedicine.disease_causeBioinformaticsGenomePathology and Forensic Medicineresistance03 medical and health sciences0302 clinical medicineCarcinoma Non-Small-Cell LungGeneticsHumansMedicineEpidermal growth factor receptorLiquid biopsyLung cancerMolecular Biologycobas®Mutationliquid biopsybiologyReverse Transcriptase Polymerase Chain Reactionbusiness.industryMolecular pathologymedicine.diseaseTKIErbB Receptors030104 developmental biology030220 oncology & carcinogenesisCancer researchbiology.proteinMolecular Medicinecompanion diagnosticHuman medicineReagent Kits DiagnosticPersonalized medicinemutationbusinessCompanion diagnosticExpert Review of Molecular Diagnostics
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Genome-wide profiling of non-smoking-related lung cancer cells reveals common RB1 rearrangements associated with histopathologic transformation in EG…

2020

The etiology and the molecular basis of lung adenocarcinomas (LuADs) in nonsmokers are currently unknown. Furthermore, the scarcity of available primary cultures continues to hamper our biological understanding of non-smoking-related lung adenocarcinomas (NSK-LuADs). We established patient-derived cancer cell (PDC) cultures from metastatic NSK-LuADs, including two pairs of matched EGFR-mutant PDCs before and after resistance to tyrosine kinase inhibitors (TKIs), and then performed whole-exome and RNA sequencing to delineate their genomic architecture. For validation, we analyzed independent cohorts of primary LuADs. In addition to known non-smoker-associated alterations (e.g. RET, ALK, EGFR…

0301 basic medicineLung NeoplasmsEGFRUbiquitin-Protein LigasesAdenocarcinoma of Lungmedicine.disease_cause03 medical and health sciences0302 clinical medicineGermline mutationtyrosine kinase inhibitorsmedicineGenetic predispositionHumanswhole-exome sequencingLung cancerGeneProtein Kinase InhibitorsExome sequencingMutationbusiness.industryEGFR RB1 lung adenocarcinoma nonsmokers tyrosine kinase inhibitors whole-exome sequencingHematologyrespiratory systemmedicine.diseaselung adenocarcinomadigestive system diseasesrespiratory tract diseasesErbB ReceptorsRetinoblastoma Binding Proteins030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellMutationCancer researchbusinessRB1Tyrosine kinaseMicrotubule-Associated Proteinsnonsmokers
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