Search results for "Platelet-Derived Growth Factor Beta"

showing 10 items of 14 documents

The PDGFRβ/ERK1/2 pathway regulates CDCP1 expression in triple-negative breast cancer

2018

Background CDCP1, a transmembrane protein with tumor pro-metastatic activity, was recently identified as a prognostic marker in TNBC, the most aggressive breast cancer subtype still lacking an effective molecular targeted therapy. The mechanisms driving CDCP1 over-expression are not fully understood, although several stimuli derived from tumor microenvironment, such as factors present in Wound Healing Fluids (WHFs), reportedly increase CDCP1 levels. Methods The expression of CDCP1, PDGFRβ and ERK1/2cell was tested by Western blot after stimulation of MDA-MB-231 cells with PDGF-BB and, similarly, in presence or not of ERK1/2 inhibitor in a panel of TNBC cell lines. Knock-down of PDGFRβ was e…

0301 basic medicineCancer ResearchMAP Kinase Signaling SystemCDCP1medicine.medical_treatmentPDGFRβPDGF-BBBecaplerminTriple Negative Breast NeoplasmsBiologylcsh:RC254-282Targeted therapyReceptor Platelet-Derived Growth Factor beta03 medical and health sciences0302 clinical medicineFISHDownregulation and upregulationWestern blotAntigens CDAntigens NeoplasmCell Line TumorGeneticsmedicineHumansRNA Small InterferingReceptorTriple-negative breast cancerMitogen-Activated Protein Kinase 1Tumor microenvironmentMitogen-Activated Protein Kinase 3ERK1/2medicine.diagnostic_testMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensNeoplasm ProteinsUp-RegulationGene Expression Regulation Neoplastic030104 developmental biologyOncologyGene Knockdown Techniques030220 oncology & carcinogenesisCDCP1Cancer researchImmunohistochemistryFemaleCell Adhesion MoleculesTNBCResearch ArticleIHCBMC Cancer
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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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Imatinib spares cKit-expressing prostate neuroendocrine tumors, whereas kills seminal vesicle epithelial-stromal tumors by targeting PDGFR-β

2017

Abstract Prostate cancer is a leading cause of cancer-related death in males worldwide. Indeed, advanced and metastatic disease characterized by androgen resistance and often associated with neuroendocrine (NE) differentiation remains incurable. Using the spontaneous prostate cancer TRAMP model, we have shown that mast cells (MCs) support in vivo the growth of prostate adenocarcinoma, whereas their genetic or pharmacologic targeting favors prostate NE cancer arousal. Aiming at simultaneously targeting prostate NE tumor cells and MCs, both expressing the cKit tyrosine kinase receptor, we have tested the therapeutic effect of imatinib in TRAMP mice. Imatinib-treated TRAMP mice experience a pa…

0301 basic medicineMaleCancer ResearchReceptor tyrosine kinaseAntineoplastic AgentProstate cancerMice0302 clinical medicineProstatebiologySeminal VesiclesImmunohistochemistryGene Expression Regulation NeoplasticNeuroendocrine TumorsProto-Oncogene Proteins c-kitmedicine.anatomical_structureOncology030220 oncology & carcinogenesisImatinib MesylateFemaleNeuroendocrine Tumormedicine.drugTrampHumanSignal TransductionPCA3medicine.medical_specialtyStromal cellXenograft Model Antitumor AssayProtein Kinase InhibitorAntineoplastic AgentsMice TransgenicReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesInternal medicineSeminal VesiclemedicineAnimalsHumansProtein Kinase InhibitorsAnimalProstatic NeoplasmsImatinibBiomarkermedicine.diseaseXenograft Model Antitumor AssaysDisease Models Animal030104 developmental biologyEndocrinologyImatinib mesylateProstatic Neoplasmbiology.proteinCancer researchBiomarkers
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miR-9 and miR-200 regulate PDGFRβ-mediated endothelial differentiation of tumor cells in triple-negative breast cancer

2016

Abstract Organization of cancer cells into endothelial-like cell-lined structures to support neovascularization and to fuel solid tumors is a hallmark of progression and poor outcome. In triple-negative breast cancer (TNBC), PDGFRβ has been identified as a key player of this process and is considered a promising target for breast cancer therapy. Thus, we aimed at investigating the role of miRNAs as a therapeutic approach to inhibit PDGFRβ-mediated vasculogenic properties of TNBC, focusing on miR-9 and miR-200. In MDA-MB-231 and MDA-MB-157 TNBC cell lines, miR-9 and miR-200 promoted and inhibited, respectively, the formation of vascular-like structures in vitro. Induction of endogenous miR-9…

0301 basic medicinePathologymedicine.medical_specialtyCancer ResearchCellular differentiationBlotting WesternFluorescent Antibody TechniqueTriple Negative Breast NeoplasmsMice SCIDBiologySettore MED/08 - Anatomia PatologicaPolymerase Chain ReactionNeovascularizationReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesMice0302 clinical medicinemicroRNAmedicineAnimalsHumansTriple-negative breast cancerIn Situ HybridizationRegulation of gene expressionNeovascularization PathologicCancerEndothelial CellsCell Differentiationmedicine.diseaseImmunohistochemistryGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologyOncologyOncology; Cancer Research030220 oncology & carcinogenesisGene Knockdown TechniquesCancer cellCancer researchHeterograftsEctopic expressionFemalemedicine.symptom
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Kosaki overgrowth syndrome: A novel pathogenic variant in PDGFRB and expansion of the phenotype including cerebrovascular complications

2020

Heterozygous activating variants in platelet-derived growth factor, beta (PDGFRB) are associated with phenotypes including Kosaki overgrowth syndrome (KOGS), Penttinen syndrome and infantile myofibromatosis (IM). Here, we present three new cases of KOGS, including a patient with a novel de novo variant c.1477A > T p.(Ser493Cys), and the oldest known individual age 53 years. The KOGS phenotype includes characteristic facial features, tall stature, scoliosis, hyperelastic thin skin, lipodystrophy, variable intellectual and neurological deterioration, and abnormalities on brain imaging. Long-term outcome is unknown. Our cases confirm the phenotypic spectrum includes progressive flexion contrac…

AdultMale0301 basic medicinePathologymedicine.medical_specialtyInfantile myofibromatosisPDGFRBScoliosis030105 genetics & heredityCraniosynostosisReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesCamptodactylyGeneticsmedicineHumansJoint dislocationStrokeGrowth DisordersGenetics (clinical)business.industryGenetic VariationMiddle Agedmedicine.diseaseCerebrovascular DisordersPhenotype030104 developmental biologymedicine.symptomLipodystrophybusinessClinical Genetics
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Growth factor concentrations and their placental mRNA expression are modulated in gestational diabetes mellitus: possible interactions with macrosomia

2009

Abstract Background Gestational diabetes mellitus (GDM) is a form of diabetes that occurs during pregnancy. GDM is a well known risk factor for foetal overgrowth, termed macrosomia which is influenced by maternal hypergycemia and endocrine status through placental circulation. The study was undertaken to investigate the implication of growth factors and their receptors in GDM and macrosomia, and to discuss the role of the materno-foeto-placental axis in the in-utero regulation of foetal growth. Methods 30 women with GDM and their 30 macrosomic babies (4.75 ± 0.15 kg), and 30 healthy age-matched pregnant women and their 30 newborns (3.50 ± 0.10 kg) were recruited in the present study. Serum …

Adultmedicine.medical_specialtyTunisiaendocrine system diseasesOffspringPlacentalcsh:Gynecology and obstetricsFetal MacrosomiaReceptor Platelet-Derived Growth Factor betaGrowth factor receptorEpidermal growth factorPregnancyPlacentaDiabetes mellitusInternal medicineResearch articleObstetrics and GynaecologyFetal macrosomiamedicineHumansRNA MessengerInsulin-Like Growth Factor Ilcsh:RG1-991PregnancyEpidermal Growth Factorbusiness.industryInfant NewbornObstetrics and Gynecologynutritional and metabolic diseasesmedicine.diseasefemale genital diseases and pregnancy complicationsUp-RegulationGestational diabetesDiabetes Gestationalmedicine.anatomical_structureEndocrinologyInsulin-Like Growth Factor Binding Protein 3Case-Control StudiesGrowth HormoneIntercellular Signaling Peptides and ProteinsFemaleFibroblast Growth Factor 2businessBMC Pregnancy and Childbirth
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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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Co-expression of receptor tyrosine kinases in esophageal adenocarcinoma and squamous cell cancer.

2008

This study aimed to define the co-expression pattern of target receptor tyrosine kinases (RTKs) in human esophageal adenocarcinoma and squamous cell cancer. The co-expression pattern of vascular endothelial growth factor receptor (VEGFR)1-3, platelet-derived growth factor receptor (PDGFR)alpha/beta and epidermal growth factor receptor 1 (EGFR1) was analyzed by RT-PCR in 50 human esophageal cancers (35 adenocarcinomas and 15 squamous cell cancers). In addition, IHC staining was applied for the confirmation of the expression and analysis of RTK localisation. The adenocarcinoma samples revealed VEGFR1 (97%), VEGFR2 (94%), VEGFR3 (77%), PDGFRalpha (91%), PDGFRbeta (85%) and EGFR1 (97%) expressi…

Cancer ResearchPathologymedicine.medical_specialtyReceptor Platelet-Derived Growth Factor alphaEsophageal NeoplasmsAdenocarcinomaReceptor tyrosine kinaseReceptor Platelet-Derived Growth Factor betaGrowth factor receptormedicineHumansEpidermal growth factor receptorVascular Endothelial Growth Factor Receptor-1biologyOncogeneCancerReceptor Protein-Tyrosine KinasesGeneral Medicinemedicine.diseaseVascular Endothelial Growth Factor Receptor-3ImmunohistochemistryVascular Endothelial Growth Factor Receptor-2ErbB ReceptorsOncologyEpidermoid carcinomacardiovascular systembiology.proteinCancer researchCarcinoma Squamous CellAdenocarcinomaPlatelet-derived growth factor receptorOncology reports
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Preclinical and clinical evidence of activity of pazopanib in solitary fibrous tumour

2014

Abstract Background To explore the activity of pazopanib in solitary fibrous tumour (SFT). Patients and methods In a preclinical study, we compared the activity of pazopanib, sorafenib, sunitinib, regorafenib, axitinib and bevacizumab in a dedifferentiated-SFT (DSFT) xenotransplanted into Severe Combined Immunodeficiency (SCID) mice. Antiangiogenics were administered at their reported optimal doses when mean tumour volume (TV) was 80 mm3. Drug activity was assessed as TV inhibition percentage (TVI%). From May 2012, six consecutive patients with advanced SFT received pazopanib, on a national name-based programme. In one case sunitinib was administered after pazopanib failure. Results In the …

Chemotherapy; Pazopanib; Sarcoma; Solitary fibrous tumour; Sunitinib; Tyrosine kinase; Administration Oral; Adult; Aged; Angiogenesis Inhibitors; Animals; Antibodies Monoclonal Humanized; Antineoplastic Agents; Bevacizumab; Humans; Imidazoles; Indazoles; Indoles; MAP Kinase Signaling System; Male; Mice SCID; Middle Aged; Neoplasm Transplantation; Niacinamide; Phenylurea Compounds; Pyridines; Pyrimidines; Pyrroles; Receptor Platelet-Derived Growth Factor beta; Solitary Fibrous Tumors; Sulfonamides; Transplantation Heterologous; Vascular Endothelial Growth Factor Receptor-2; Cancer Research; Oncology; Medicine (all)OncologyMaleCancer ResearchIndolesAxitinibPyridinesPyridinemedicine.medical_treatmentSolitary fibrous tumourAdministration OralAngiogenesis InhibitorsMice SCIDPharmacologyPyrroleAntineoplastic Agentchemistry.chemical_compoundMiceSolitary Fibrous TumorChemotherapy; Pazopanib; Sarcoma; Solitary fibrous tumour; Sunitinib; Tyrosine kinase; Cancer Research; Oncology; Medicine (all)Transplantation HeterologouMonoclonalSunitinibHumanizedSulfonamidesHeterologousSunitinibMedicine (all)ImidazolesSarcomaMiddle AgedSorafenibPlatelet-Derived Growth Factor betaAxitinibBevacizumabOncologySolitary Fibrous TumorsAdministrationAngiogenesis InhibitorHumanmedicine.drugReceptorPhenylurea CompoundSorafenibOralAdultNiacinamidemedicine.medical_specialtyIndazolesBevacizumabMAP Kinase Signaling SystemTransplantation HeterologousAntineoplastic AgentsSulfonamideAntibodies Monoclonal HumanizedSCIDAntibodiesReceptor Platelet-Derived Growth Factor betaPazopanibInternal medicineRegorafenibmedicineAnimalsHumansChemotherapyPyrrolesImidazoleTyrosine kinaseAgedChemotherapyTransplantationAnimalbusiness.industryPhenylurea CompoundsPazopanibmedicine.diseaseChemotherapy; Pazopanib; Sarcoma; Solitary fibrous tumour; Sunitinib; Tyrosine kinase; Administration Oral; Adult; Aged; Angiogenesis Inhibitors; Animals; Antibodies Monoclonal Humanized; Antineoplastic Agents; Axitinib; Bevacizumab; Humans; Imidazoles; Indazoles; Indoles; MAP Kinase Signaling System; Male; Mice SCID; Middle Aged; Neoplasm Transplantation; Niacinamide; Phenylurea Compounds; Pyridines; Pyrimidines; Pyrroles; Receptor Platelet-Derived Growth Factor beta; Solitary Fibrous Tumors; Sorafenib; Sulfonamides; Sunitinib; Transplantation Heterologous; Vascular Endothelial Growth Factor Receptor-2Vascular Endothelial Growth Factor Receptor-2IndazolePyrimidinesPyrimidinechemistryIndolebusinessProgressive diseaseNeoplasm Transplantation
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A germline mutation in the platelet-derived growth factor receptor beta gene may be implicated in hereditary progressive mucinous histiocytosis.

2020

DermatologyBiologymedicine.diseaseSkin DiseasesReceptor Platelet-Derived Growth Factor betaHistiocytosisGermline mutationChronic diseaseHereditary progressive mucinous histiocytosisChronic DiseaseCancer researchmedicinePlatelet-Derived Growth Factor Receptor BetaHumansPlatelet-Derived Growth Factor BetaReceptorGeneHistiocytosisGerm-Line Mutation
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