Search results for "Growth factor"

showing 10 items of 1300 documents

Apoptosis and the liver

2000

Regulation of the homeostatic balance between cell proliferation and programmed cell death, apoptosis, is essential for development and maintenance of multicellular organisms. Apoptosis is a genetically and evolutionarily highly conserved process. Analysis of the molecular mechanisms of apoptosis has led to a better understanding of many human diseases. Notably in cancer, but also in infectious or autoimmune disease, a deficiency in apoptosis is one of the key events in pathophysiology. On the other hand, overefficient apoptosis, as observed in fulminant liver failure, may be equally harmful for the organism indicating that a tight regulation of the apoptotic machinery is essential for surv…

Cancer ResearchProgrammed cell deathCeramideHepatitis Viral HumanDNA damageCellGenes mycApoptosisBiologyReceptors Tumor Necrosis Factorchemistry.chemical_compoundmedicineHumansfas ReceptorLiver DiseasesLiver NeoplasmsIntrinsic apoptosisGenes p53Genes bcl-2Liver TransplantationCell biologymedicine.anatomical_structureLiverchemistryUVB-induced apoptosisApoptosisImmunologyPoly(ADP-ribose) PolymerasesSignal transductionReceptors Transforming Growth Factor betaSeminars in Cancer Biology
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Effects of interferon gamma on the proliferation and modulation of cell-surface structures of human ovarian carcinoma cell lines.

1993

Platinum-containing regimens are very effective in the primary treatment of ovarian cancer. However, upon subsequent treatment most tumors develop multidrug resistance. The clinical application of biological response modifiers like interferon gamma (IFN gamma) in advanced ovarian cancer is therefore of increasing interest. Permanent ovarian cancer cell lines are suitable for investigating the mode of action and the potential clinical effectiveness of such response modifiers. IFN gamma is known to modulate many cellular functions. In this study it was compared for its antiproliferative and antigen-modulatory activity on the expression of tumor-associated (CA-125, HMFG, CEA) and major histoco…

Cancer ResearchReceptor expressionCellInterferon-gammaAntigenEpidermal growth factorAntigens NeoplasmHLA AntigensMHC class ImedicineTumor Cells CulturedHumansAntigens Tumor-Associated CarbohydrateOvarian NeoplasmsMHC class IIbiologyCell growthCell MembraneGeneral Medicinemedicine.diseaseRecombinant ProteinsErbB ReceptorsGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyImmunologyAntigens Surfacebiology.proteinCancer researchFemaleOvarian cancerCell DivisionJournal of cancer research and clinical oncology
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Platelet-derived growth factor alpha mediates the proliferation of peripheral T-cell lymphoma cells via an autocrine regulatory pathway.

2014

Peripheral T-cell lymphomas not otherwise specified (PTCL/NOS) are very aggressive tumors characterized by consistent aberrant expression of platelet-derived growth factor receptor alpha (PDGFRA). In this study, we aimed to identify the determinants of PDGFRA activity in PTCL/NOS and to elucidate the biological consequences of its activation. We observed overexpression of the PDGFRA gene by gene expression profiling in most of the tested PTCLs and confirmed the expression of PDGFRA and phospho-PDGFRA using immunohistochemistry. The integrity of the PDFGRA locus was demonstrated using several different approaches, including massive parallel sequencing and Sanger sequencing. PDGF-AA was found…

Cancer ResearchReceptor Platelet-Derived Growth Factor alphamedicine.medical_treatmentT celltumor cell proliferationPDGFRAGrowth factor receptorCell Line TumormedicinePDFGRASTAT5 Transcription FactorHumansAutocrine signallingExtracellular Signal-Regulated MAP KinasesSTAT5PTCL/NOS; PDFGRA; tumor cell proliferationCell ProliferationPlatelet-Derived Growth FactorbiologyCell growthExtracellular Signal-Regulated MAP KinaseGrowth factorLymphoma T-Cell PeripheralHematologyPTCL/NOSdigestive system diseasesGene expression profilingAutocrine Communicationmedicine.anatomical_structureAnesthesiology and Pain MedicineSTAT1 Transcription FactorOncologyCancer researchbiology.proteinT-cell lymphomaProto-Oncogene Proteins c-aktHuman
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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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Tumor-intrinsic and -extrinsic roles of c-Kit: mast cells as the primary off-target of tyrosine kinase inhibitors.

2011

c-Kit tyrosine kinase receptor and its ligand stem cell factor have multiple functions during development, whereas in adulthood they are mostly needed for stem cell (SC) maintenance and mast cell (MC) biology. c-Kit plays an essential tumor-cell-intrinsic role in many types of cancer, either providing the tumorigenic force when aberrantly activated or conferring stem-like features characterizing the most aggressive variants. A tumor-cell-extrinsic role occurs through c-Kit-dependent accessory cells (such as MCs) that infiltrate tumors and deeply influence their progression. c-Kit-targeted therapy with tyrosine kinase inhibitors (TKIs) may ideally work against both tumor and stromal cells. H…

Cancer ResearchStromal cellStem cell factorAntineoplastic AgentsBiologyc-kit; mast cells; mouse mutants; off-target; tyrosine kinase inhibitorsReceptor tyrosine kinaseMicec-KitNeoplasmstyrosine kinase inhibitorsGeneticsmedicineAnimalsHumansNeoplasm InvasivenessMast CellsMolecular BiologyProtein Kinase InhibitorsStem Cell Factormouse mutantsNeovascularization PathologicMast cellRatsProto-Oncogene Proteins c-kitmedicine.anatomical_structureTumor progressionmast cells.biology.proteinCancer researchStem cellTyrosine kinasePlatelet-derived growth factor receptoroff-targetMastocytosisOncogene
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Results from a phase III trial (GRID) evaluating regorafenib (REG) in metastatic gastrointestinal stromal tumour (GIST): Subgroup analysis of outcome…

2013

10551 Background: REG, an oral receptor kinase inhibitor with activity against KIT, PDGFR, VEGFR, FGFRs, and other oncologic targets, demonstrated significant improvement in progression-free survival (PFS) over placebo (PL) in a phase III study (GRID) of patients (pts) with advanced GIST following failure of at least imatinib (IM) and sunitinib (SU). To understand the impact of pts’ baseline characteristics on outcome, we performed an exploratory analysis of REG effects across pt subgroups based on sex, age, and mitotic index of primary GIST tissue, as well as duration and number of lines of previous therapies. Methods: Adult pts with metastatic GIST (n=199) progressing after at least IM a…

Cancer ResearchStromal cellbiologyGiSTKinasebusiness.industryVEGF receptorsSubgroup analysischemistry.chemical_compoundOncologychemistryRegorafenibbiology.proteinCancer researchMedicineReceptorbusinessPlatelet-derived growth factor receptor
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Abstract B290: Activation of the PD-1 pathway contributes to immune escape in EGFR-driven lung tumors.

2013

Abstract The recent clinical success of therapeutic blockade of the immune checkpoint Programmed Death (PD)-1 in advanced lung cancer patients suggests that mechanisms of immune escape may contribute to lung tumor pathogenesis. We identified a correlation between Epidermal Growth Factor Receptor (EGFR) pathway activation and a gene signature indicative of immunosuppression manifested by upregulation of PD-1, PD-L1, cytotoxic T lymphocyte antigen-4 (CTLA-4) and multiple tumor-promoting inflammatory cytokines. Accordingly, we identified a decrease in the number of cytotoxic T cells and an increase in markers of T cell exhaustion in genetically engineered mouse models (GEMMs) of EGFR-driven lu…

Cancer ResearchTumor microenvironmentbiologyCell growthT cellCancermedicine.diseaseImmune checkpointmedicine.anatomical_structureOncologyImmunologybiology.proteinmedicineCytotoxic T cellEpidermal growth factor receptorLung cancerMolecular Cancer Therapeutics
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Analysis of Antiproliferative and Chemosensitizing Effects of Sunitinib on Human Esophagogastric Cancer Cells: Synergistic Interaction With Vandetani…

2009

The receptor tyrosine kinases (RTKs), epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor 1-3 (VEGFR1-3), are frequently expressed in gastric cancer and are putative therapeutic targets in this disease. We have investigated the anti-proliferative and chemosensitizing properties of the multitargeted small-molecule RTK inhibitors sunitinib and vandetanib in a panel of 4 human gastric and esophageal cancer cell lines. In the 1st instance, the expression of potential targets of these small-molecule inhibitors was examined by reverse transcriptase-polymerase chain reaction, western blotting, and flow cytometry. EGFR mRNA and protein was detected in all cases, …

Cancer ResearchUmbilical VeinsIndolesEsophageal NeoplasmsApoptosisVandetanibTyrosine-kinase inhibitorReceptor tyrosine kinasechemistry.chemical_compoundPiperidinesSunitinibMedicineDrug InteractionsEpidermal growth factor receptorPhosphorylationCells CulturedbiologySunitinibReverse Transcriptase Polymerase Chain ReactionDrug SynergismFlow CytometryErbB ReceptorsOncologyPhosphorylationDrug Therapy Combinationmedicine.drugSignal Transductionmedicine.medical_specialtymedicine.drug_classBlotting WesternAntineoplastic AgentsStomach NeoplasmsInternal medicineHumansPyrrolesPropidium iodideRNA MessengerProtein Kinase InhibitorsCell ProliferationVascular Endothelial Growth Factor Receptor-1business.industryCancermedicine.diseaseVascular Endothelial Growth Factor Receptor-3Vascular Endothelial Growth Factor Receptor-2EndocrinologychemistryCancer researchbiology.proteinQuinazolinesEndothelium VascularbusinessProto-Oncogene Proteins c-akt
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Parthenolide generates reactive oxygen species and autophagy in MDA-MB231 cells. A soluble parthenolide analogue inhibits tumour growth and metastasi…

2013

Triple-negative breast cancers (TNBCs) are clinically aggressive forms associated with a poor prognosis. We evaluated the cytotoxic effect exerted on triple-negative MDA-MB231 breast cancer cells both by parthenolide and its soluble analogue dimethylamino parthenolide (DMAPT) and explored the underlying molecular mechanism. The drugs induced a dose- and time-dependent decrement in cell viability, which was not prevented by the caspase inhibitor z-VAD-fmk. In particular in the first hours of treatment (1–3 h), parthenolide and DMAPT strongly stimulated reactive oxygen species (ROS) generation. The drugs induced production of superoxide anion by activating NADPH oxidase. ROS generation caused…

Cancer ResearchautophagyCell SurvivalparthenolideFas-Associated Death Domain ProteinImmunologyCASP8 and FADD-Like Apoptosis Regulating ProteinBreast Neoplasmsparthenolide; ROS; NOX; autophagy; breast cancer xenograft.MiceCellular and Molecular Neurosciencechemistry.chemical_compoundDownregulation and upregulationCell Line TumorSettore BIO/10 - BiochimicaAnimalsHumansParthenolidePropidium iodidebreast cancer xenograftMembrane Potential Mitochondrialchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologybreast cancer xenograft.SuperoxideNF-kappa BRNA-Binding ProteinsROSCell BiologyNOXXenograft Model Antitumor AssaysMolecular biologyNuclear Pore Complex ProteinsVascular endothelial growth factorchemistryCell cultureCancer researchbiology.proteinCalciumFemaleOriginal ArticleReactive Oxygen SpeciesSesquiterpenes
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Resistance to epidermal growth factor receptor inhibition in non-small cell lung cancer

2018

Cancer Researchbiologybusiness.industryAfatiniblung cancer EGFR epidermal growth factor receptor inhibition resistancemedicine.diseaseEGFR Tyrosine Kinase InhibitorsGefitinibCancer researchbiology.proteinMedicinePharmacology (medical)OsimertinibEpidermal growth factor receptorErlotinibNon small cellbusinessLung cancermedicine.drug
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