Search results for "Growth factor"

showing 10 items of 1300 documents

MDA-MB-231 and 8701BC breast cancer lines promote the migration and invasiveness of ECV304 cells on 2D and 3D type-I collagen matrix

2017

Tumor angiogenesis is a multiphasic process, having the extracellular matrix remodeling as critical step. Different classes of proteolytic enzymes in matrix digestion/remodeling are involved. The role of lytic enzymes and their activation mode have not been completely elucidated. Herein, the crosstalk between endothelia and tumor cells, by realization of bi- and three-dimensional endothelial and breast cancer cells co-cultures, were studied in vitro. Particularly, the effects of two tumor conditioned media (TCM) were assessed about endothelial proliferation, migration, and invasiveness. An increase in expression of pro-MMP9 was detected when endothelial cells were cultured in the presence o…

0301 basic medicineMMP2Proteolytic enzymesCell migrationCell BiologyGeneral MedicineMatrix metalloproteinaseBiologyMMP7Extracellular matrix03 medical and health sciencesVascular endothelial growth factor A030104 developmental biology0302 clinical medicine030220 oncology & carcinogenesisImmunologyCancer researchMMP14Cell Biology International
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Elevated Serum Fibroblast Growth Factor 21 in Humans with Acute Pancreatitis.

2016

Background The metabolic regulator Fibroblast Growth Factor 21 (FGF21) is highly expressed in the acinar pancreas, but its role in pancreatic function is obscure. It appears to play a protective role in acute experimental pancreatitis in mice. The aim of this study was to define an association between FGF21 and the course and resolution of acute pancreatitis in humans. Methods and Principal Findings Twenty five subjects with acute pancreatitis admitted from May to September 2012 to the Beth Israel Deaconess Medical Center (BIDMC) were analyzed. Serial serum samples were collected throughout hospitalization and analyzed for FGF21 levels by ELISA. Twenty healthy subjects sampled three times o…

0301 basic medicineMaleAbdominal painFGF21Fibroblast Growth FactorPhysiologyHydrolaseslcsh:MedicineFibroblast growth factorPathology and Laboratory MedicineGastroenterologyBiochemistryEndocrinologyMedicine and Health SciencesLipasesIsraellcsh:ScienceFluidsMultidisciplinaryLiver DiseasesPhysicsFatty liverMiddle AgedEnzymesmedicine.anatomical_structurePhysical SciencesAcute DiseaseAcute pancreatitisFemalemedicine.symptomAnatomyPancreasResearch Articlemedicine.medical_specialtyStates of MatterPainEndocrine SystemGastroenterology and Hepatology03 medical and health sciencesExocrine GlandsSigns and SymptomsDiagnostic MedicineInternal medicineGrowth FactorsmedicineEndocrine systemHumansPancreasDemographyEndocrine Physiologybusiness.industrylcsh:RBiology and Life SciencesProteinsmedicine.diseaseAbdominal PainFatty LiverFibroblast Growth Factors030104 developmental biologyEndocrinologyPancreatitisPeople and PlacesEnzymologyPancreatitislcsh:QbusinessPLoS ONE
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Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.

2019

Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of…

0301 basic medicineMaleCancer ResearchBiopsyL-amp GB EGFR-low amplified glioblastomamedicine.disease_causewt wildtypeMYBPC3 myosin-binding protein C0302 clinical medicineHIC1 hypermethylated in cancer 1Gene duplicationIn Situ Hybridization FluorescenceIDH2 isocitrate dehydrogenase 2MutationRB-pat RB signaling pathwayEGFRvIII epidermal growth factor receptor variant number IIIPAH phenylalanine hydroxylaseGBM glioblastoma IDH-wildtype (glioblastoma multiforme primary glioblastoma).ANOVA ANalysis Of VArianceN-amp GB EGFR-no amplified glioblastomaMiddle AgedCDKN2A cyclin-dependent kinase inhibitor 2Alcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisPrimary tumorImmunohistochemistryH-amp GB EGFR-high amplified glioblastomaErbB ReceptorsTKR-pat tyrosine-kinase receptors signaling pathway030220 oncology & carcinogenesisDisease ProgressionCDK6 cyclin-dependent kinase 6CDH1 Cadherin 1FemaleCREM cAMP response element modulatorIHC immunohistochemistryAdultOriginal articleDNA Copy Number VariationsCDKN1B cyclin-dependent kinase inhibitor 1BBiologyRARB retinoic acid receptor betaCNS central nervous systemlcsh:RC254-282IDH1 isocitrate dehydrogenase 1BCL2 B-cell cll/ lymphoma 2CNAs copy number algerationsWHO World Health Organization03 medical and health sciencesYoung Adultp53-pat p53 signaling pathwaymedicineBiomarkers TumorTMA tissue microarrayPTENHumansProtein kinase BPI3K/AKT/mTOR pathwaySurvival analysisAgedGenetic heterogeneityGene AmplificationGFAP glial fibrillary acidic proteinMLPA multiplex ligation-dependent probe amplificationmedicine.diseaseFISH fluorescence in situ hibridizationSurvival AnalysisCDKN2B cyclin-dependent kinase inhibitor 2BPTEN phosphatase and tensin homologEGFR epidermal growth factor receptorCNV-load load of copy number variations030104 developmental biologyMutationPARK2 parkinCancer researchbiology.proteinTCGA The Cancer Genome AtlasLARGE1 acetylglucosaminyltransferase-like protein 1GlioblastomaCHD7 Chromodomain Helicase DNA Binding Protein 7DAPI 4′6-diamidino-2-phenylindoleNeoplasia (New York, N.Y.)
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BRG1/SMARCA4 is essential for neuroblastoma cell viability through modulation of cell death and survival pathways.

2016

Neuroblastoma (NB) is a neoplasm of the sympathetic nervous system, and is the most common solid tumor of infancy. NBs are very heterogeneous, with a clinical course ranging from spontaneous regression to resistance to all current forms of treatment. High-risk patients need intense chemotherapy, and only 30-40% will be cured. Relapsed or metastatic tumors acquire multi-drug resistance, raising the need for alternative treatments. Owing to the diverse mechanisms that are responsible of NB chemoresistance, we aimed to target epigenetic factors that control multiple pathways to bypass therapy resistance. We found that the SWI/SNF-related, matrix-associated, actin-dependent regulator of chromat…

0301 basic medicineMaleCancer ResearchCombination therapyCell SurvivalBiologyMolecular oncologyTranscriptome03 medical and health sciencesNeuroblastomaPhosphatidylinositol 3-Kinases0302 clinical medicineGrowth factor receptorNeuroblastomaCell Line TumorGeneticsmedicineHumansMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell ProliferationCell DeathDNA HelicasesNuclear ProteinsCell cyclemedicine.diseaseGene Expression Regulation Neoplastic030104 developmental biologyProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisImmunologyCancer researchFemaleTranscriptomeSignal TransductionTranscription FactorsOncogene
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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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Meta-analysis identifies novel risk loci and yields systematic insights into the biology of male-pattern baldness

2017

Male-pattern baldness (MPB) is a common and highly heritable trait characterized by androgen-dependent, progressive hair loss from the scalp. Here, we carry out the largest GWAS meta-analysis of MPB to date, comprising 10,846 early-onset cases and 11,672 controls from eight independent cohorts. We identify 63 MPB-associated loci (P<5 × 10−8, METAL) of which 23 have not been reported previously. The 63 loci explain ∼39% of the phenotypic variance in MPB and highlight several plausible candidate genes (FGF5, IRF4, DKK2) and pathways (melatonin signalling, adipogenesis) that are likely to be implicated in the key-pathophysiological features of MPB and may represent promising targets for the de…

0301 basic medicineMaleCandidate genegenetics [Trans-Activators]SRD5A2 protein humanMedizinGeneral Physics and Astronomygenetics [3-Oxo-5-alpha-Steroid 4-Dehydrogenase]Genome-wide association studyBioinformatics0302 clinical medicinegenetics [Interferon Regulatory Factors]GenotypeMelatoninGeneticsMultidisciplinaryAdipogenesisEBF1 protein humanintegumentary systemgenetics [Intercellular Signaling Peptides and Proteins]QPhenotypeFGF5 protein humangenetics [Membrane Proteins]Phenotype030220 oncology & carcinogenesisMeta-analysisUrological cancers Radboud Institute for Health Sciences [Radboudumc 15]Interferon Regulatory FactorsIntercellular Signaling Peptides and ProteinsMale-pattern baldnessddc:500Signal TransductionDKK2 protein humanGenotypeFibroblast Growth Factor 53-Oxo-5-alpha-Steroid 4-Dehydrogenase/genetics; Adipogenesis/genetics; Alopecia/genetics; Case-Control Studies; Fibroblast Growth Factor 5/genetics; Genetic Association Studies; Genome-Wide Association Study; Genotype; Humans; Intercellular Signaling Peptides and Proteins/genetics; Interferon Regulatory Factors/genetics; Male; Melatonin; Membrane Proteins/genetics; Phenotype; Signal Transduction/genetics; Trans-Activators/geneticsScienceGenomicsBiologygenetics [Signal Transduction]General Biochemistry Genetics and Molecular BiologyArticle03 medical and health sciencesinterferon regulatory factor-43-Oxo-5-alpha-Steroid 4-DehydrogenasemedicineHumansgenetics [Adipogenesis]Genetic Association Studiesgenetics [Alopecia]Case-control studyMembrane ProteinsAlopeciaGeneral Chemistrymedicine.diseasegenetics [Fibroblast Growth Factor 5]030104 developmental biologyCase-Control StudiesTrans-ActivatorsGenome-Wide Association Study
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Cannabinoid receptor expression in non-small cell lung cancer. Effectiveness of tetrahydrocannabinol and cannabidiol inhibiting cell proliferation an…

2020

Background/Objective Patients with non-small cell lung cancer (NSCLC) develop resistance to antitumor agents by mechanisms that involve the epithelial-to-mesenchymal transition (EMT). This necessitates the development of new complementary drugs, e.g., cannabinoid receptors (CB1 and CB2) agonists including tetrahydrocannabinol (THC) and cannabidiol (CBD). The combined use of THC and CBD confers greater benefits, as CBD enhances the effects of THC and reduces its psychotropic activity. We assessed the relationship between the expression levels of CB1 and CB2 to the clinical features of a cohort of patients with NSCLC, and the effect of THC and CBD (individually and in combination) on prolifer…

0301 basic medicineMaleCannabinoid receptorLung NeoplasmsPulmonologymedicine.medical_treatmentGene ExpressionBiochemistryLung and Intrathoracic TumorsReceptor Cannabinoid CB20302 clinical medicineContractile ProteinsReceptor Cannabinoid CB1Epidermal growth factorCarcinoma Non-Small-Cell LungMedicine and Health SciencesCannabidiolDronabinolAged 80 and overMultidisciplinaryChemistryQRDrugsMiddle AgedCancer Cell MigrationCell MotilityOncologyCell Processes030220 oncology & carcinogenesisMedicinelipids (amino acids peptides and proteins)Femalemedicine.drugResearch ArticleAdultEpithelial-Mesenchymal TransitionScienceChronic Obstructive Pulmonary DiseaseCell Migration03 medical and health sciencesCell Line Tumormental disordersmedicineGeneticsHumansEpithelial–mesenchymal transitionTetrahydrocannabinolCell ProliferationAgedA549 cellPharmacologyCannabinoid Receptor AgonistsPsychotropic DrugsCell growthCannabinoidsorganic chemicalsCancers and NeoplasmsBiology and Life SciencesProteinsCell Biologydigestive system diseasesActinsrespiratory tract diseasesNon-Small Cell Lung CancerCytoskeletal Proteins030104 developmental biologyA549 CellsCancer researchCannabinoidCannabidiolDevelopmental BiologyPLoS ONE
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Urinary- and Plasma-Derived Exosomes Reveal a Distinct MicroRNA Signature Associated With Albuminuria in Hypertension.

2021

Urinary albumin excretion (UAE) is a marker of cardiovascular risk and renal damage in hypertension. MicroRNAs (miRNAs) packaged into exosomes function as paracrine effectors in cell communication and the kidney is not exempt. This study aimed to state an exosomal miRNA profile/signature associated to hypertension with increased UAE and the impact of profibrotic TGF-β1 (transforming growth factor β1) on exosomes miRNA release. Therefore, exosomes samples from patients with hypertension with/without UAE were isolated and characterized. Three individual and unique small RNA libraries from each subject were prepared (total plasma, urinary, and plasma-derived exosomes) for next-generation sequ…

0301 basic medicineMaleDown-Regulation030204 cardiovascular system & hematologyExosomesTransforming Growth Factor beta103 medical and health sciencesParacrine signalling0302 clinical medicinemicroRNAInternal MedicinemedicineAlbuminuriaHumansGene Regulatory NetworksKEGGCells CulturedAgedKidneybusiness.industryPodocytesReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingMiddle AgedMicrovesiclesMicroRNAs030104 developmental biologyReal-time polymerase chain reactionmedicine.anatomical_structureHypertensionAlbuminuriaCancer researchFemalemedicine.symptombusinessTransforming growth factorHypertension (Dallas, Tex. : 1979)
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The significance of epidermal growth factor receptor uncommon mutations in non-small cell lung cancer: A systematic review and critical appraisal

2020

Uncommon epidermal growth factor receptor (EGFR) mutations collectively account for 10% of EGFR mutations, harboring heterogeneous molecular alterations within exons 18-21 with clinically variable responses to EGFR tyrosine kinase inhibitors (TKIs) in advanced Non-Small Cell Lung Cancer (NSCLC) patients. In addition, with the introduction of different NGS gene approach an improvement of EGFR mutations detection was reported. Today, no specific studies have prospectively evaluated uncommon sensitizing mutations in detail and no firm standard of care has been established in the first-line setting. The aim of this comprehensive review is to critically consider the clinical role of uncommon EGF…

0301 basic medicineMaleLung NeoplasmsPrognosiEGFRProtein Kinase Inhibitormedicine.disease_causeNSCLC03 medical and health sciencesExonErbB Receptors0302 clinical medicineCarcinoma Non-Small-Cell LungmedicineCarcinomaHumansRadiology Nuclear Medicine and imagingEpidermal growth factor receptorErbB ReceptorLung cancerGeneProtein Kinase InhibitorsRegulation of gene expressionMutationbiologybusiness.industryGeneral Medicinemedicine.diseasePrognosisTKIUncommon mutationErbB ReceptorsGene Expression Regulation NeoplasticLung Neoplasm030104 developmental biologyTreatment OutcomeOncology030220 oncology & carcinogenesisNGSMutationCancer researchbiology.proteinSystematic reviewFemalebusinessHuman
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Fasciola hepatica reinfection potentiates a mixed Th1/Th2/Th17/Treg response and correlates with the clinical phenotypes of anemia.

2016

Background: Fascioliasis is a severe zoonotic disease of worldwide extension caused by liver flukes. In human fascioliasis hyperendemic areas, reinfection and chronicity are the norm and anemia is the main sign. Herein, the profile of the Th1/Th2/Th17/Treg expression levels is analyzed after reinfection, correlating them with their corresponding hematological biomarkers of morbidity. Methodology/Principal findings: The experimental design reproduces the usual reinfection/chronicity conditions in human fascioliasis endemic areas and included Fasciola hepatica primo-infected Wistar rats (PI) and rats reinfected at 8 weeks (R8), and at 12 weeks (R12), and negative control rats. In a cross-sect…

0301 basic medicineMalePhysiologymedicine.medical_treatmentSnailslcsh:MedicineGene ExpressionImmune PhysiologyGene expressionMedicine and Health Scienceslcsh:ScienceImmune ResponseInnate Immune SystemMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionFOXP3hemic and immune systemsImmunosuppressionEBI3AnemiaForkhead Transcription FactorsHematologyThymusInterleukin-10Interleukin 10medicine.anatomical_structureHelminth InfectionsCytokinesResearch ArticleNeglected Tropical DiseasesFascioliasisImmunologychemical and pharmacologic phenomenaSpleenBiologyTransforming Growth Factor beta103 medical and health sciencesImmune systemTh2 CellsGeneticsParasitic DiseasesmedicineFasciola hepaticaAnimalsRats WistarCell ProliferationInterleukinslcsh:RBiology and Life SciencesMolecular DevelopmentFasciola hepaticaTh1 CellsTropical Diseasesbiology.organism_classificationRats030104 developmental biologyCross-Sectional StudiesImmune SystemImmunologyTh17 Cellslcsh:QSpleenDevelopmental Biology
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