Search results for " Fibroblasts"

showing 10 items of 47 documents

Microenvironment in neuroblastoma: isolation and characterization of tumor-derived mesenchymal stromal cells

2018

Background It has been proposed that mesenchymal stromal cells (MSCs) promote tumor progression by interacting with tumor cells and other stroma cells in the complex network of the tumor microenvironment. We characterized MSCs isolated and expanded from tumor tissues of pediatric patients diagnosed with neuroblastomas (NB-MSCs) to define interactions with the tumor microenvironment. Methods Specimens were obtained from 7 pediatric patients diagnosed with neuroblastoma (NB). Morphology, immunophenotype, differentiation capacity, proliferative growth, expression of stemness and neural differentiation markers were evaluated. Moreover, the ability of cells to modulate the immune response, i.e. …

0301 basic medicineMaleRegistrieCancer ResearchCellular differentiationMesenchymal stromal cellsCell SeparationNeuroblastoma0302 clinical medicineImmunophenotypingCancer-Associated FibroblastsTumor MicroenvironmentCytotoxic T cellRegistriesStemnessCancer-Associated FibroblastCoculture TechniqueChildrenCells CulturedStemneChemistryMesenchymal stromal cellCell CycleEMTCell Differentiationlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensImmunohistochemistryMesenchymal Stem CellOncology030220 oncology & carcinogenesisChild PreschoolPopulation SurveillanceBone Marrow CellFemaleResearch ArticleHumanSignal TransductionStromal cellMicroenvironmentBone Marrow Cellslcsh:RC254-282Immunophenotyping03 medical and health sciencesGeneticsBiomarkers TumorHumansSettore MED/04 - Patologia GeneraleTumor microenvironmentGene Expression ProfilingMesenchymal stem cellInfantMesenchymal Stem CellsCoculture Techniques030104 developmental biologyTumor progressionCancer cellMutationCancer research
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Differential subcellular expression of P525LFUS as a putative biomarker for ALS phenoconversion

2020

P525LFused-in-Sarcoma ( FUS ) mutation is associated with a specific amyotrophic lateral sclerosis (ALS) phenotype characterized by a juvenile-onset and a severe course.1 This harmful point mutation is located in the nuclear localization signal (NLS) domain at the protein C-terminal.2 Although wild-type FUS protein is expressed almost exclusively in the nucleus, the P525L FUS mutation leads to a protein mislocalization into the cytoplasm3,4 because of its loss of capacity to bind its transporter karyopherin-2 and to be transferred back to the nucleus.3

0301 basic medicineMutationPoint mutationTransporterALS FUS fibroblastsBiologymedicine.disease_causemedicine.diseasePhenotypeCell biology03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structuremedicineNLSSettore MED/26 - NeurologiaNeurology (clinical)Amyotrophic lateral sclerosisNucleus030217 neurology & neurosurgeryGenetics (clinical)Nuclear localization sequence
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Neuroblastoma patient-derived orthotopic xenografts reflect the microenvironmental hallmarks of aggressive patient tumours.

2016

AbstractTreatment of high-risk childhood neuroblastoma is a clinical challenge which has been hampered by a lack of reliable neuroblastoma mouse models for preclinical drug testing. We have previously established invasive and metastasising patient-derived orthotopic xenografts (PDXs) from high-risk neuroblastomas that retained the genotypes and phenotypes of patient tumours. Given the important role of the tumour microenvironment in tumour progression, metastasis, and treatment responses, here we analysed the tumour microenvironment of five neuroblastoma PDXs in detail. The PDXs resembled their parent tumours and retained important stromal hallmarks of aggressive lesions including rich bloo…

0301 basic medicinePathologymedicine.medical_specialtyCancer ResearchStromal cellGenotypeTumour stromaBiologyPolymorphism Single NucleotideMetastasisMetastasisPaediatric cancer03 medical and health sciencesMiceNeuroblastoma0302 clinical medicineNeuroblastomamedicineTumor MicroenvironmentAnimalsHumansPatient-derived xenograft (PDX)Tumor microenvironmentTumour microenvironmentNeovascularization Pathologicmedicine.diseaseXenograft Model Antitumor AssaysDisease Models Animal030104 developmental biologyLymphatic systemOncology030220 oncology & carcinogenesisCancer-Associated FibroblastsImmunohistochemistryBlood VesselsChildhood NeuroblastomaCancer letters
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TNFSF14 (LIGHT) Exhibits Inflammatory Activities in Lung Fibroblasts Complementary to IL-13 and TGF-β

2018

The cytokine TNFSF14 [homologous to Lymphotoxin, exhibits Inducible expression and competes with HSV Glycoprotein D for binding to HVEM, a receptor expressed on T lymphocytes (LIGHT)] has been shown in mouse models to be important for development of lung tissue remodeling that is characteristic of asthma, idiopathic pulmonary fibrosis (IPF), and systemic sclerosis (SSc). However, its cellular targets are not fully delineated. In the present report, we show that LTβR and HVEM, the receptors for LIGHT, are constitutively expressed in primary human lung fibroblasts (HLFs). We asked whether LIGHT could promote inflammatory and remodeling-relevant activity in HLFs and how this was similar to, or…

0301 basic medicinelcsh:Immunologic diseases. AllergyTGF-βChemokineTumor Necrosis Factor Ligand Superfamily Member 14medicine.medical_treatmentImmunologyGene ExpressionInflammationProinflammatory cytokineCell Line03 medical and health sciences0302 clinical medicineTransforming Growth Factor betamedicineImmunology and AllergyHumansLungCells CulturedOriginal ResearchCell ProliferationInterleukin-13biologyChemistrylung fibroblastsasthmaFibroblasts3. Good healtha receptor expressed on T lymphocytes030104 developmental biologyCytokineLymphotoxinCXCL5030220 oncology & carcinogenesisIL-13Interleukin 13biology.proteinCancer researchCytokinesexhibits Inducible expression and competes with HSV Glycoprotein D for binding to HVEMmedicine.symptomhomologous to LymphotoxinInflammation Mediatorslcsh:RC581-607MyofibroblastBiomarkersFrontiers in Immunology
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Ataluren for the Treatment of Usher Syndrome 2A Caused by Nonsense Mutations

2019

The identification of genetic defects that underlie inherited retinal diseases (IRDs) paves the way for the development of therapeutic strategies. Nonsense mutations caused approximately 12% of all IRD cases, resulting in a premature termination codon (PTC). Therefore, an approach that targets nonsense mutations could be a promising pharmacogenetic strategy for the treatment of IRDs. Small molecules (translational read-through inducing drugs

0301 basic medicinepatient-derived fibroblastsUsher syndromechemistry.chemical_compound0302 clinical medicineMedicineTRIDSpectroscopyCells CulturedExtracellular Matrix ProteinsOxadiazolesGeneral MedicinePhenotypeImmunohistochemistryComputer Science ApplicationsRetinitis pigmentosaCodon Nonsenseocular therapyUsher syndromeUsher SyndromesNonsense mutationModels BiologicalCatalysisArticleInorganic Chemistry03 medical and health sciencesStructure-Activity RelationshipAtalurenCiliogenesisparasitic diseasesRetinitis pigmentosaHumansGenetic Predisposition to DiseasePhysical and Theoretical ChemistryMolecular BiologyGenetranslational read-throughbusiness.industryOrganic ChemistryHEK 293 cellsFibroblastsmedicine.diseaseAtaluren030104 developmental biologyHEK293 CellschemistryProtein BiosynthesisMutationCancer researchbusiness030217 neurology & neurosurgeryInternational Journal of Molecular Sciences
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Positive effects of an extracellular matrix hydrogel on rat anterior cruciate ligament fibroblast proliferation and collagen mRNA expression

2015

Summary Background/Objective We have previously shown that an extracellular matrix (ECM) bioscaffold derived from porcine small intestine submucosa (SIS) enhanced the healing of a gap injury of the medial collateral ligament as well as the central third defect of the patellar tendon. With the addition of a hydrogel form of SIS, we found that a transected goat anterior cruciate ligament (ACL) could also be healed. The result begs the research question of whether SIS hydrogel has positive effects on ACL fibroblasts (ACLFs) and thus facilitates ACL healing. Methods In the study, ECM-SIS hydrogel was fabricated from the digestion of decellularised and sterilised sheets of SIS derived from αGal-…

ACL fibroblasts; Fibre morphology; Growth factors; Hydrogel; Porcine small intestine submucosa; Orthopedics and Sports Medicinelcsh:Diseases of the musculoskeletal systemfibre morphologyAnterior cruciate ligamentExtracellular matrixchemistry.chemical_compoundgrowth factorsmedicineOrthopedics and Sports MedicineBovine serum albuminFibroblastporcine small intestine submucosabiologyCell growthAnatomyGrowth factorACL fibroblastsACL fibroblastMolecular biologymedicine.anatomical_structurechemistrySelf-healing hydrogelsbiology.proteinOriginal Articlelcsh:RC925-935hydrogelBromodeoxyuridineExplant cultureJournal of Orthopaedic Translation
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CAF-like state in primary skin fibroblasts with constitutional BRCA1 epimutation sheds new light on tumor suppressor deficiency-related changes in he…

2016

Constitutive epimutations of tumor suppressor genes are increasingly considered as cancer predisposing factors equally to sequence mutations. In light of the emerging role of the microenvironment for cancer predisposition, initiation, and progression, we aimed to characterize the consequences of a BRCA1 epimutation in cells of mesenchymal origin. We performed a comprehensive molecular and cellular comparison of primary dermal fibroblasts taken from a monozygous twin pair discordant for recurrent cancers and BRCA1 epimutation, whose exceptional clinical case we previously reported in this journal. Comparative transcriptome analysis identified differential expression of extracellular matrix-r…

Adult0301 basic medicineCancer ResearchTwinsHaploinsufficiencyKetone BodiesExtracellular matrixTranscriptome03 medical and health sciencesCell Line TumormedicineHumansGenes Tumor SuppressorMolecular BiologyPDPNCells CulturedOligonucleotide Array Sequence AnalysisSkinExtracellular Matrix ProteinsbiologyBRCA1 ProteinCell growthGenes HomeoboxCancerDNA MethylationFibroblastsmedicine.diseaseGene Expression Regulation Neoplastic030104 developmental biologyCulture Media ConditionedMutationDNA methylationImmunologyCancer researchbiology.proteinCytokinesCancer-Associated FibroblastsFemaleNeoplasm Recurrence LocalACTA2TranscriptomeResearch PaperEpigenetics
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CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis.

2014

SummaryCancer stem cells drive tumor formation and metastasis, but how they acquire metastatic traits is not well understood. Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors. CD44v6 expression is low in primary tumors but demarcated clonogenic CR-CSC populations. Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis. CD44v6− progenitor cells do not give rise to metastatic lesions but, when…

CA15-3Animals; Biomarkers Tumor; Bone Morphogenetic Proteins; Carcinogenesis; Colonic Neoplasms; Fibroblasts; Humans; Hyaluronan Receptors; Mice SCID; Neoplasm Metastasis; Neoplasm Proteins; Neoplastic Stem Cells; Phosphatidylinositol 3-Kinases; Prognosis; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-met; Signal Transduction; Treatment Outcome; Wnt Proteins; Cellular Reprogramming; Molecular Medicine; Genetics; Cell BiologyCarcinogenesisWnt ProteinMice SCIDmedicine.disease_causeAnimals; Antigens CD44; Biomarkers Tumor; Bone Morphogenetic Proteins; Carcinogenesis; Colonic Neoplasms; Fibroblasts; Humans; Mice SCID; Neoplasm Metastasis; Neoplasm Proteins; Neoplastic Stem Cells; Phosphatidylinositol 3-Kinases; Prognosis; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-met; Signal Transduction; Treatment Outcome; Wnt Proteins; Cellular ReprogrammingMetastasisMicePhosphatidylinositol 3-KinasesCD44Neoplasm MetastasisCarcinogenesiPhosphoinositide-3 Kinase InhibitorsColonic NeoplasmTumorbiologyProto-Oncogene Proteins c-metCellular ReprogrammingPrognosisAntigens CD44Neoplasm ProteinsNeoplasm MetastasiAnimals; Antigens CD44; Biomarkers Tumor; Bone Morphogenetic Proteins; Carcinogenesis; Colonic Neoplasms; Fibroblasts; Humans; Mice SCID; Neoplasm Metastasis; Neoplasm Proteins; Neoplastic Stem Cells; Phosphatidylinositol 3-Kinases; Prognosis; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-met; Signal Transduction; Treatment Outcome; Wnt Proteins; Cellular Reprogramming; Cell Biology; Molecular Medicine; GeneticsHyaluronan ReceptorsTreatment OutcomeBone Morphogenetic ProteinsColonic NeoplasmsNeoplastic Stem CellsFibroblastMolecular MedicineHepatocyte growth factorStem cellHumanmedicine.drugSignal TransductionPrognosiProtein Kinase InhibitorSCIDNeoplasm ProteinCancer stem cellSettore MED/04 - PATOLOGIA GENERALEmedicineGeneticsBiomarkers TumorAnimalsHumansAntigensProgenitor cellProtein Kinase InhibitorsSettore MED/04 - Patologia GeneraleAnimalBone Morphogenetic Proteincancer metastasisCD44Cell BiologyFibroblastsmedicine.diseaseWnt ProteinsSettore MED/18 - Chirurgia GeneraleImmunologyCancer researchbiology.proteinNeoplastic Stem CellPhosphatidylinositol 3-KinaseCarcinogenesisBiomarkersCell stem cell
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Tumor and its microenvironment: a synergistic interplay.

2013

The mutual and interdependent interaction between tumor and its microenvironment is a crucial topic in cancer research. Recently, it was reported that targeting stromal events could improve efficacies of current therapeutics and prevent metastatic spreading. Tumor microenvironment is a "complex network" of different cell types, soluble factors, signaling molecules and extracellular matrix components, which orchestrate the fate of tumor progression. As by definition, cancer stem cells (CSCs) are proposed to be the unique cell type able to maintain tumor mass and survive outside the primary tumor at metastatic sites. Being exposed to environmental stressors, including reactive oxygen species …

Cancer ResearchStromal cellEpithelial-Mesenchymal TransitionAngiogenesisCell SurvivalBiologyCancer stem cellCell MovementNeoplasmsmedicineTumor MicroenvironmentAnimalsHumansEpithelial–mesenchymal transitionNeoplasm MetastasisStem Cell NicheHypoxiaTumor microenvironmentNeovascularization Pathologicmedicine.diseaseAngiogenesis CAFs CAMs CRC CSCs ECM EMT GSH HIF Hypoxia MMPs ROS Tumor microenvironment VEGF cancer stem cells cancer-associated fibroblasts cancer-associated macrophages colorectal cancer epithelial mesenchymal transition extracellular matrix hypoxia-inducible factor matrix metalloproteinase reactive oxygen species reduced glutathione vascular endothelial growth factorPrimary tumorTumor progressionImmunologyCancer researchNeoplastic Stem CellsCancer-Associated FibroblastsOxidation-ReductionSignal Transduction
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Human HSP10 variants downregulation after cigarette smoke extract exposure in lung cells

2009

The impact of cigarette-smoke stress (a form of oxidative stress) on human lung fibroblasts and epithelial cells, particularly its effect on Hsp10 expression, has not been characterized despite the fact that a role for mitochondrial chaperonins in the development of lung diseases, ranging from chronic obstructive pulmonary disease to bronchial carcinogenesis, has been suggested (1). We studied the effects of non-lethal doses of cigarette smoke extract (CSE) on the expression of Hsp10 in human lung fibroblasts (HFL-1 line) and epithelial cells (16HBE line). Proteomics was carried out using 2D-IPG, silver stain, western blotting, and mass-spectrometry; mRNA was measured by RT-PCR. Database se…

Hsp10 cigarette smoke bronchial epithelial cells lung fibroblasts oxidative stress 2D-electrophoresis IPG isoelectric variants chaperoninsSettore BIO/16 - Anatomia Umana
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