Search results for "Growth factor"

showing 10 items of 1300 documents

p53 and p53-related mediators PAI-1 and IGFBP-3 are downregulated in peripheral blood mononuclear cells of HIV-patients exposed to non-nucleoside rev…

2019

The improved effectiveness and safety of the combined antiretroviral therapy (cART) has largely diminished mortality and AIDS-defining morbidity of HIV-patients. Nevertheless, chronic age-related diseases in these individuals are more common and their underlying pathogenic mechanisms of these actions seem to involve accelerated aging and enhanced inflammation. The present study explores markers of these processes in a heterogenous Spanish HIV cohort using peripheral blood samples of HIV-patients and matched uninfected controls. We isolated periheral blood mononuclear cells (PBMCs) and i) compared the expression of a panel of 14 genes related to inflammation and senescence in PBMCs of HIV-pa…

0301 basic medicineSenescenceAdultMaleAnti-HIV Agents030106 microbiologyDown-RegulationInflammationHIV InfectionsCCL2Peripheral blood mononuclear cell03 medical and health sciencesVirologyAntiretroviral Therapy Highly ActivePlasminogen Activator Inhibitor 1medicineCXCL10HumansCellular SenescencePharmacologyInflammationbusiness.industryInterleukin-6Interleukin-18virus diseasesMiddle AgedCCL20Chemokine CXCL10030104 developmental biologyInsulin-Like Growth Factor Binding Protein 3ImmunologyLeukocytes MononuclearReverse Transcriptase InhibitorsInterleukin 18Tumor necrosis factor alphaFemalemedicine.symptomTumor Suppressor Protein p53businessAntiviral research
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PCSK9-D374Y mediated LDL-R degradation can be functionally inhibited by EGF-A and truncated EGF-A peptides: An in vitro study.

2019

Abstract Background and aims Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to low density lipoprotein receptor (LDLR) through the LDLR epidermal growth factor-like repeat A (EGF-A) domain and induces receptor internalization and degradation. PCSK9 has emerged as a novel therapeutic target for hypercholesterolemia. Clinical studies with PCSK9 inhibiting antibodies have demonstrated strong LDL-c lowering effects, but other therapeutic approaches using small molecule inhibitors for targeting PCSK9 functions may offer supplementary therapeutic options. The aim of our study was to evaluate the effect of synthetic EGF-A analogs on mutated (D374Y) PCSK9-D374Y mediated LDLR degradatio…

0301 basic medicineSmall peptidesmedia_common.quotation_subject030204 cardiovascular system & hematologyDecoy strategyPCSK903 medical and health sciences0302 clinical medicineHumansInternalizationCells Culturedmedia_commonExpression vectorEpidermal Growth FactorChemistryPCSK9PCSK9 InhibitorsTransfectionProprotein convertasePCSK9 inhibitionIn vitroCell biologyEGF-A domain030104 developmental biologyLDLRReceptors LDLLDL receptorMutationKexinlipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineAtherosclerosis
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A phase 2 study of galunisertib (TGF-Β R1 inhibitor) and sorafenib in patients with advanced hepatocellular carcinoma (HCC).

2017

4097 Background: TGFβ signaling is associated with HCC progression. Inhibition of TGFβ R1 potentiates activity of sorafenib in in-vitro and in-vivo models. Here we report the clinical activity of galunisertib (G) plus sorafenib (S) in pts with incurable HCC and no prior systemic therapy. Methods: Eligibility criteria included incurable HCC with measurable disease per RECIST 1.1, no prior systemic therapy, Child Pugh A, ECOG PS ≤1.G was administered as 80 mg PO BID (lead-in Cohort 1) or 150 mg PO BID (lead-in Cohort 2 and expansion cohort), as intermittent dosing of 14 days on/off (28 days = 1 cycle). S was administered continuously as a 400 mg PO BID. Primary objective was to characterize …

0301 basic medicineSorafenibCancer ResearchPathologymedicine.medical_specialtybusiness.industryPhases of clinical researchmedicine.disease03 medical and health sciences030104 developmental biology0302 clinical medicineOncology030220 oncology & carcinogenesisHepatocellular carcinomaCancer researchMedicineGalunisertibIn patientbusinessTransforming growth factormedicine.drugJournal of Clinical Oncology
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Multikinase inhibitors sorafenib and sunitinib as radiosensitizers in head and neck cancer cell lines

2017

Background Radioresistance is a common feature of head and neck squamous cell carcinoma (HNSCC). We previously showed that the irradiation- activated vascular endothelial growth factor (VEGF)-extracellular signal-regulated kinase (ERK)-axis is fundamental for the survival of resistant tumors. In this study, we examined if treatment with potent multikinase (MK) inhibitors, sorafenib and sunitinib, could radiosensitize tumor cells. Methods Cultured HNSCC cell lines were treated with inhibitors and subsequently irradiated. Radiosensitizing effects were functionally assessed by annexin-V apoptosis and clonogenic assays and confirmed by Western blot. Additionally, we surveyed human HNSCC tissue …

0301 basic medicineSorafenibMAPK/ERK pathwaySunitinibbusiness.industrymedicine.diseaseHead and neck squamous-cell carcinomaVascular endothelial growth factor03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicineOtorhinolaryngologychemistry030220 oncology & carcinogenesisRadioresistancemedicineCancer researchRadiosensitizing AgentClonogenic assaybusinessmedicine.drugHead & Neck
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Chronic myelogenous leukaemia exosomes modulate bone marrow microenvironment through activation of epidermal growth factor receptor

2016

Abstract Chronic myelogenous leukaemia (CML) is a clonal myeloproliferative disorder. Recent evidence indicates that altered crosstalk between CML and mesenchymal stromal cells may affect leukaemia survival; moreover, vesicles released by both tumour and non‐tumour cells into the microenvironment provide a suitable niche for cancer cell growth and survival. We previously demonstrated that leukaemic and stromal cells establish an exosome‐mediated bidirectional crosstalk leading to the production of IL8 in stromal cells, thus sustaining the survival of CML cells. Human cell lines used are LAMA84 (CML cells), HS5 (stromal cells) and bone marrow primary stromal cells; gene expression and protei…

0301 basic medicineStromal cellchronic myeloid leukaemiaEGFRBone Marrow CellsexosomesBiologyInterleukin 8AmphiregulinBone Marrow Stromal Cell03 medical and health sciencesAmphiregulinSettore BIO/13 - Biologia Applicatahemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineCell AdhesionHumansInterleukin 8Epidermal growth factor receptorRNA MessengerPhosphorylationRNA Small InterferingAnnexin A2SNAILMesenchymal stem cellInterleukin-8Cell BiologyOriginal ArticlesMicrovesiclesCell biologyErbB Receptors030104 developmental biologymedicine.anatomical_structureCellular MicroenvironmentMatrix Metalloproteinase 9Cancer cellChronic Myelogenous Leukemia Exosomes; Interleukin 8; Bone Marrow Stromal Cells; EGFRbiology.proteinMolecular MedicineOriginal ArticleBone marrowSnail Family Transcription FactorsChronic Myelogenous Leukemia ExosomeStromal Cellsepidermal growth factor receptor
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MET/HGF Co-Targeting in Pancreatic Cancer: A Tool to Provide Insight into the Tumor/Stroma Crosstalk

2018

The ‘onco-receptor’ MET (Hepatocyte Growth Factor Receptor) is involved in the activation of the invasive growth program that is essential during embryonic development and critical for wound healing and organ regeneration during adult life. When aberrantly activated, MET and its stroma-secreted ligand HGF (Hepatocyte Growth Factor) concur to tumor onset, progression, and metastasis in solid tumors, thus representing a relevant target for cancer precision medicine. In the vast majority of tumors, wild-type MET behaves as a ‘stress-response’ gene, and relies on ligand stimulation to sustain cancer cell ‘scattering’, invasion, and protection form apoptosis. …

0301 basic medicineStromal cellpancreatic cancerReviewHGF; MET; Metastasis; Pancreatic cancer; Target therapy; Tumor microenvironment; Animals; Hepatocyte Growth Factor; Humans; Neoplasm Metastasis; Pancreatic Neoplasms; Proto-Oncogene Proteins c-metCatalysisMetastasisInorganic Chemistrylcsh:Chemistry03 medical and health sciences0302 clinical medicinePancreatic cancermedicineAnimalsHumansmetastasistumor microenvironmentHGFPhysical and Theoretical ChemistryNeoplasm MetastasisMolecular Biologylcsh:QH301-705.5SpectroscopyTumor microenvironmentbusiness.industryHepatocyte Growth Factortarget therapyOrganic ChemistryGeneral MedicineProto-Oncogene Proteins c-metmedicine.diseaseComputer Science ApplicationsPancreatic Neoplasms030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Tumor progressionHepatocyte Growth Factor Receptor030220 oncology & carcinogenesisCancer cellCancer researchMETHepatocyte growth factorbusinessmedicine.drugInternational Journal of Molecular Sciences
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Identification of neuronal and angiogenic growth factors in an in vitro blood-brain barrier model system: Relevance in barrier integrity and tight ju…

2016

We previously demonstrated that the co-cultivation of endothelial cells with neural cells resulted in an improved integrity of the in vitro blood-brain barrier (BBB), and that this model could be useful to evaluate the transport properties of potential central nervous system disease drugs through the microvascular brain endothelial. In this study we have used real-time PCR, fluorescent microscopy, protein arrays and enzyme-linked immunosorbent assays to determine which neural- and endothelial cell-derived factors are produced in the co-culture and improve the integrity of the BBB. In addition, a further improvement of the BBB integrity was achieved by adjusting serum concentrations and grow…

0301 basic medicineSus scrofaCell Culture TechniquesCell CommunicationBiologyMatrix metalloproteinaseBlood–brain barrierBiochemistryTight JunctionsCapillary Permeability03 medical and health sciences0302 clinical medicinePEDFIn vivoNeurotrophic factorsCell Line TumormedicineElectric ImpedanceAnimalsHumansNerve Growth FactorsAngiogenic ProteinsNeuronsTight Junction ProteinsTight junctionEndothelial CellsCell BiologyCoculture TechniquesCell biologyVascular endothelial growth factor B030104 developmental biologymedicine.anatomical_structurePhenotypeBlood-Brain BarrierImmunologyNeurovascular CouplingEndostatinCardiology and Cardiovascular Medicine030217 neurology & neurosurgerySignal TransductionMicrovascular research
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Alternative Splice Forms of CYLD Mediate Ubiquitination of SMAD7 to Prevent TGFB Signaling and Promote Colitis

2018

Background & Aims The CYLD lysine 63 deubiquitinase gene (CYLD) encodes tumor suppressor protein that is mutated in familial cylindromatosus, and variants have been associated with Crohn disease (CD). Splice forms of CYLD that lack exons 7 and 8 regulate transcription factors and functions of immune cells. We examined the expression of splice forms of CYLD in colon tissues from patients with CD and their effects in mice. Methods We performed immunohistochemical analyses of colon tissues from patients with untreated CD and patients without inflammatory bowel diseases (controls). We obtained mice that expressed splice forms of CYLD (sCYLD mice) without or with SMAD7 (sCYLD/SMAD7 mice) from tr…

0301 basic medicineTranscription FactorBiopsyInbred C57BLTransgenicImmune RegulationSettore MED/12MiceRandom Allocation0302 clinical medicineCrohn DiseaseReference ValuesNeedleIntestinal Mucosaintegumentary systemChemistryBiopsy NeedleGastroenterologyT helper cellFlow CytometryPost-translational ModificationImmunohistochemistryDeubiquitinating Enzyme CYLDCysteine Endopeptidasesmedicine.anatomical_structure030211 gastroenterology & hepatologyTumor necrosis factor alphaSignal TransductionGenetically modified mouseRegulatory T cellTransgeneMice TransgenicSmad7 ProteinTransforming Growth Factor beta103 medical and health sciencesImmune systemmedicineAnimalsHumansCytokine SignalingHepatologyAnimalHEK 293 cellsUbiquitinationMolecular biologyMice Inbred C57BLDisease Models Animal030104 developmental biologyDisease ModelsCytokine Signaling; Immune Regulation; Post-translational Modification; Transcription Factor; Biopsy Needle; Crohn Disease; Cysteine Endopeptidases; Deubiquitinating Enzyme CYLD; Disease Models Animal; Flow Cytometry; Immunohistochemistry; Intestinal Mucosa; Mice Inbred C57BL; Mice Transgenic; Random Allocation; Reference Values; Signal Transduction; Smad7 Protein; Transforming Growth Factor beta1; UbiquitinationTransforming growth factorGastroenterology
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11q Deletion or ALK Activity Curbs DLG2 Expression to Maintain an Undifferentiated State in Neuroblastoma

2020

High-risk 11q deleted neuroblastomas typically display undifferentiated/poorly differentiated morphology. Neuroblastoma is thought to develop from Schwann cell precursors and undifferentiated neural crest (NC) derived cells. It is therefore vital to understand mechanisms involved in the block of differentiation. We identify an important role for oncogenic ALK-ERK1/2-SP1 signaling in maintenance of undifferentiated NC-derived progenitors via repression of DLG2, a tumor suppressor in neuroblastoma. DLG2 is expressed in the ‘bridge signature’ that represents the transcriptional transition state when neural crest cells or Schwann Cell Precursors become chromaffin cells of the adrenal gland. We …

0301 basic medicineTranscription GeneticCarcinogenesisChromaffin CellsRetinoic acidlaw.inventionNeuroblastomachemistry.chemical_compound0302 clinical medicinelawNerve Growth FactorMedicine and Health Sciencesretinoic acidAnaplastic Lymphoma Kinaselcsh:QH301-705.5NeuronsMice Inbred BALB CNeural crestCell DifferentiationPrognosisCandidate Tumor Suppressor GeneDLG2Up-RegulationCell biologyGene Expression Regulation NeoplasticERKPhenotypeTreatment Outcomemedicine.anatomical_structureFemaleChromosome Deletiontumor suppressorMAP Kinase Signaling SystemSp1 Transcription FactorSchwann cellGenetics and Molecular BiologyTretinoinBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesAdrenergic AgentsCell Line TumorNeuroblastomamedicineAnimalsHumansProgenitor cellGenePsychological repressionCell ProliferationChromosomes Human Pair 11Tumor Suppressor Proteinsmedicine.disease030104 developmental biologyALKlcsh:Biology (General)chemistryTrk receptorGeneral BiochemistrySuppressorSchwann CellsGuanylate Kinases030217 neurology & neurosurgerySSRN Electronic Journal
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AB052. P-20. Phase 2, open-label study of second-line M7824 treatment in patients with locally advanced or metastatic biliary tract cancer

2019

BACKGROUND: Transforming growth factor β (TGF-β) signaling promotes tumor immunosuppression; its inhibition in the tumor microenvironment may enhance the response to anti-PD-L1 treatment. M7824 is an innovative first-in-class bifunctional fusion protein composed of 2 extracellular domains of TGF-βRII (a TGF-β “trap”) fused to a human IgG1 mAb against PD-L1. Building upon encouraging efficacy observed in a phase 1 study, the present study will evaluate M7824 clinical benefit in patients with pretreated biliary tract cancer (BTC). METHODS: This multicenter, international trial is evaluating M7824 monotherapy in patients with locally advanced or metastatic (LA/M) BTC unselected for tumor PD-L1…

0301 basic medicineTumor microenvironmentBiliary tract cancerbiologybusiness.industrymedicine.drug_classMonoclonal antibodyFusion protein03 medical and health sciences030104 developmental biology0302 clinical medicine030220 oncology & carcinogenesisPD-L1Poster AbstractsCancer researchExtracellularbiology.proteinMedicineIn patientbusinessTransforming growth factor
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