Search results for "FIBROBLAST"

showing 10 items of 667 documents

Preclinical and Clinical Characterization of Fibroblast-derived Neuregulin-1 on Trastuzumab and Pertuzumab Activity in HER2-positive Breast Cancer.

2021

[Purpose]: To characterize expression of neuregulin-1 (NRG1), an HER3 ligand, in HER2-positive breast cancer and its relation with the efficacy of trastuzumab with or without pertuzumab.

Cancer ResearchStromal cellReceptor ErbB-2medicine.medical_treatmentNeuregulin-1Drug Evaluation PreclinicalBreast NeoplasmsAntibodies Monoclonal HumanizedBreast cancerAntineoplastic Agents ImmunologicalTrastuzumabAntineoplastic Combined Chemotherapy Protocolsmental disordersmedicineTumor Cells CulturedHumansNeuregulin 1skin and connective tissue diseasesneoplasmsNeoadjuvant therapyRetrospective Studiesbiologybusiness.industryFibroblastsTrastuzumabmedicine.diseasebody regionsTreatment OutcomeOncologyCancer cellbiology.proteinCancer researchImmunohistochemistryFemalePertuzumabbusinessmedicine.drug
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MYCN and survivin cooperatively contribute to malignant transformation of fibroblasts

2013

The oncogenes MYCN and survivin (BIRC5) maintain aggressiveness of diverse cancers including sarcomas. To investigate whether these oncogenes cooperate in initial malignant transformation, we transduced them into Rat-1 fibroblasts. Indeed, survivin enhanced MYCN-driven contact-uninhibited and anchorage-independent growth in vitro. Importantly, upon subcutaneous transplantation into mice, cells overexpressing both instead of either one of the oncogenes generated tumors with shortened latency, marked anaplasia and an increased proliferation-to-apoptosis ratio resulting in accelerated growth. Mechanistically, the increased tumorigenicity was associated with an enhanced Warburg effect and a hyp…

Cancer ResearchSurvivinBlotting WesternApoptosisBiologyReal-Time Polymerase Chain ReactionN-Myc Proto-Oncogene ProteinInhibitor of Apoptosis ProteinsMalignant transformationImmunoenzyme TechniquesMiceAdenosine TriphosphateSurvivinmedicineAnimalsHumansLactic AcidRNA MessengerneoplasmsAnaplasiaCells CulturedCell ProliferationHomeodomain ProteinsOncogene ProteinsN-Myc Proto-Oncogene ProteinReverse Transcriptase Polymerase Chain ReactionCell growthNuclear ProteinsGeneral MedicineFibroblastsWarburg effectCell HypoxiaRatsTransplantationCell Transformation NeoplasticGlucoseHypoxia-inducible factorsCancer researchmedicine.symptomGlycolysisCarcinogenesis
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Involvement of protein kinase Cdelta in contact-dependent inhibition of growth in human and murine fibroblasts.

2001

There is evidence that protein kinase C delta (PKCdelta) is a tumor suppressor, although its physiological role has not been elucidated so far. Since important anti-proliferative signals are mediated by cell-cell contacts we studied whether PKCdelta is involved in contact-dependent inhibition of growth in human (FH109) and murine (NIH3T3) fibroblasts. Cell-cell contacts were imitated by the addition of glutardialdehyde-fixed cells to sparsely seeded fibroblasts. Downregulation of the PKC isoforms alpha, delta, epsilon, and mu after prolonged treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA, 0.1 microM) resulted in a significant release from contact-inhibition in FH109 cells. Bryosta…

Cancer ResearchTime FactorsBryostatin 1ImmunoprecipitationActive Transport Cell NucleusDown-RegulationBiologychemistry.chemical_compoundFixativesLactonesMiceDownregulation and upregulationGeneticsmedicineAnimalsHumansProtein IsoformsBenzopyransEnzyme InhibitorsFibroblastProtein kinase AMolecular BiologyProtein kinase CProtein Kinase CChemotaxisCell CycleAcetophenones3T3 CellsFibroblastsBryostatinsMolecular biologyBlotIsoenzymesProtein Kinase C-deltamedicine.anatomical_structurechemistryGlutaralTetradecanoylphorbol AcetateMacrolidesMitogensRottlerinCell DivisionProtein BindingOncogene
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Reduction of glutathione content by 12-O-tetradecanoylphorbol-13-acetate in confluent, but not in sparse cultures of human diploid fibroblasts.

1990

Treatment of confluent cultures of human diploid fibroblasts with 12-O-tetradecanoylphorbol-13-acetate (TPA) (10(-7) M) resulted in a 70% reduction of the glutathione (GSH) content, compared with untreated controls. The effect, which was dose-dependent, was observed 8 h after the beginning of the treatment could be followed for up to 72 h. On the other hand, GSH reduction was specific for confluent cultures, as the level of glutathione remained unchanged by TPA treatment of sparse cultures. The addition of immobilized plasma membrane proteins to sparsely seeded cells has been shown previously to induce cellular reactions which are characteristic for confluent cultures. It was shown that TPA…

Cancer ResearchTime FactorsCell CountGeneral MedicineGlutathioneBiologyFibroblasts12-O-Tetradecanoylphorbol-13-acetatemedicine.disease_causeMolecular biologyGlutathioneIn vitrochemistry.chemical_compoundmedicine.anatomical_structureMembrane proteinchemistryCell culturemedicineHumansTetradecanoylphorbol AcetateTumor promotionFibroblastCarcinogenesisCells CulturedCarcinogenesis
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RB acute loss induces centrosome amplification and aneuploidy in murine primary fibroblasts

2006

AbstractBackgroundIncorrect segregation of whole chromosomes or parts of chromosome leads to aneuploidy commonly observed in cancer. The correct centrosome duplication, assuring assembly of a bipolar mitotic spindle, is essential for chromosome segregation fidelity and preventing aneuploidy. Alteration of p53 and pRb functions by expression of HPV16-E6 and E7 oncoproteins has been associated with centrosome amplification. However, these last findings could be the result of targeting cellular proteins in addition to pRb by HPV16-E7 oncoprotein. To get a more detailed picture on the role of pRb in chromosomal instability and centrosome amplification, we analyzed the effects of the acute loss …

Cancer ResearchTime FactorsTranscription GeneticRbCentrosomes AneuploidyGene ExpressionMitosisAneuploidyBiologyRetinoblastoma Proteinlcsh:RC254-282Chromosome segregationMiceChromosome instabilityGene duplicationmedicineAnimalsCentrosome duplicationMitosisCells CulturedCentrosomeResearchGene AmplificationFibroblastsAneuploidylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseSettore BIO/18 - GeneticaSpindle checkpointOncologyCentrosomeCancer researchMolecular MedicineMolecular Cancer
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Partial restoration of pre-transformation levels of lysyl oxidase and transin mRNAs in phenotypic ras revertants.

1995

Neoplastic transformation mediated by ras oncogenes is associated with deregulated expression of genes encoding, for example, various proteases, lysyl oxidase, and smooth-muscle α-actin. To define the role of these genes in the initiation or maintenance of the ras-transformed state, we compared their steady-state mRNA levels in two different sets of preneoplastic fibroblast lines, ras-transformed clones, and phenotypic revertants derived from them. Compared with the preneoplastic fibroblasts, the ras-transformed derivatives exhibited elevated levels of cathepsin L (major excreted protein), transin (stromelysin I, matrix metalloproteinase–3), and collagenase I (matrix metalloproteinase–1) mR…

Cancer ResearchTranscription GeneticCathepsin LBlotting WesternGene ExpressionLysyl oxidaseCell LineCathepsin LProtein-Lysine 6-OxidaseProto-Oncogene Proteins c-mycDownregulation and upregulationEndopeptidasesmedicineAnimalsNeoplastic transformationCollagenasesRNA MessengerFibroblastMolecular BiologyGeneMessenger RNAbiologyMetalloendopeptidasesPhenotypeMolecular biologyCathepsinsNeoplasm ProteinsRatsCysteine Endopeptidasesmedicine.anatomical_structureCell Transformation NeoplasticGenes rasPhenotypebiology.proteinMatrix Metalloproteinase 3Matrix Metalloproteinase 1Precancerous ConditionsMolecular carcinogenesis
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Pharmacologic activation of p53 elicits Bax-dependent apoptosis in the absence of transcription

2003

AbstractRecent efforts to develop pharmacologic agents that restore function to mutant forms of p53 hold significant promise in cancer therapy. Here, we examine the effects of such pharmacologic activation of p53 function using a small molecule, PRIMA-1, and a model system employing a p53 protein fused to a mutant steroid binding domain of the murine estrogen receptor (p53ERtam) that renders it responsive only in the presence of 4-hydroxytamoxifen. In either case, p53 activation triggered apoptosis that was not inhibited by the presence of macromolecular synthesis inhibitors. This p53-induced, transcription-independent apoptosis is Bax dependent, proceeds in the absence of a nucleus, and in…

Cancer ResearchTranscription GeneticRecombinant Fusion ProteinsMutantEstrogen receptorApoptosis03 medical and health sciencesMice0302 clinical medicineBcl-2-associated X proteinProto-Oncogene ProteinsTumor Cells CulturedAnimalsHumansCloning MolecularReceptorCells Cultured030304 developmental biologybcl-2-Associated X ProteinCell NucleusProtein Synthesis Inhibitors0303 health sciencesAza CompoundsbiologyCytochrome cCytochromes cCell BiologyFibroblastsBridged Bicyclo Compounds Heterocyclic3. Good healthCell biologyTransport proteinMitochondriaProtein TransportTamoxifenProto-Oncogene Proteins c-bcl-2Receptors EstrogenOncologyApoptosis030220 oncology & carcinogenesisMutationbiology.proteinTumor Suppressor Protein p53Binding domainCancer Cell
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Lenvatinib (len) plus pembrolizumab (pembro) for the first-line treatment of patients (pts) with advanced hepatocellular carcinoma (HCC): Phase 3 LEA…

2019

TPS4152 Background: Len, an inhibitor of VEGF receptors 1-3, FGF receptors 1-4, PDGF receptor α, RET, and KIT, is approved for first-line treatment of unresectable HCC (uHCC) based on the open-label phase 3 REFLECT study in which len showed noninferior overall survival (OS) and significantly improved objective response rate (ORR), progression-free survival (PFS), and time-to-progression (TTP) vs sorafenib. In the phase 2 KEYNOTE-224 study of pembro (a PD-1 inhibitor) as second-line treatment of advanced HCC, pembro showed meaningful clinical efficacy in pts previously treated with sorafenib, with median PFS 4.9 mo, median OS 12.9 mo, and a manageable safety profile. In results from the pha…

Cancer Researchbiologybusiness.industryVEGF receptorsPembrolizumabFibroblast growth factormedicine.diseaseFirst line treatment03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOncologychemistry030220 oncology & carcinogenesisHepatocellular carcinomabiology.proteinCancer researchMedicineLenvatinibbusinessReceptorPlatelet-derived growth factor receptor030215 immunologyJournal of Clinical Oncology
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Geranylgeraniol - a new potential therapeutic approach to bisphosphonate associated osteonecrosis of the jaw.

2010

Bisphosphonate associated osteonecrosis of the jaw (BP-ONJ) is one of the main side effects of bisphosphonate therapy (BPT). To date, there is no effective therapy of the BP-ONJ. Nitrogen-containing bisphosphonates (N-BPs) are particularly able to inhibit pyrophosphate synthase (FPPS) in the mevalonate pathway (MVP). Consequent of decreased synthesis of the metabolite Geranylgeraniol (GGOH) is believed to largely account for the development of BP-ONJ. Negative effect of N-BPs could be shown, resulting in decreased viability and migration capacity of different cell types of hard and soft tissues such as osteoblasts, fibroblast und endothelial cells. Aim of our in vitro study was to demonstra…

Cancer Researchmedicine.medical_specialtyCell typeCellIn Vitro Techniqueschemistry.chemical_compoundGeranylgeraniolmedicineHumansFibroblastBisphosphonate-associated osteonecrosis of the jawMigration AssayOsteoblastsBone Density Conservation AgentsDiphosphonatesbusiness.industryOsteonecrosisEndothelial CellsFibroblastsmedicine.diseaseSurgerymedicine.anatomical_structureOncologychemistryCancer researchMevalonate pathwayOral SurgeryDiterpenesbusinessWound healingJaw DiseasesOral oncology
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Physiological mechanisms regulating the expression of endothelial-type NO synthase

2002

Although endothelial nitric oxide synthase (eNOS) is a constitutively expressed enzyme, its expression is regulated by a number of biophysical, biochemical, and hormonal stimuli, both under physiological conditions and in pathology. This review summarizes the recent findings in this field. Shear stress, growth factors (such as transforming growth factor-beta, fibroblast growth factor, vascular endothelial growth factor, and platelet-derived growth factor), hormones (such as estrogens, insulin, angiotensin II, and endothelin 1), and other compounds (such as lysophosphatidylcholine) upregulate eNOS expression. On the other hand, the cytokine tumor necrosis factor-alpha and bacterial lipopolys…

Cancer Researchmedicine.medical_specialtyNitric Oxide Synthase Type IIIPhysiologyRNA Stabilitymedicine.medical_treatmentClinical BiochemistryBiologyFibroblast growth factorBiochemistryGene Expression Regulation Enzymologicchemistry.chemical_compoundEnosInternal medicinemedicineAnimalsPromoter Regions GeneticRegulation of gene expressionBase SequenceGene Expression ProfilingGrowth factorbiology.organism_classificationActin cytoskeletonAngiotensin IICell biologyVascular endothelial growth factorEndocrinologychemistryNitric Oxide SynthaseSignal transductionSignal TransductionNitric Oxide
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