Search results for "Programmed cell death"

showing 10 items of 609 documents

Programmed Death Ligand 1 (PD-L1) as a Predictive Biomarker for Pembrolizumab Therapy in Patients with Advanced Non-Small-Cell Lung Cancer (NSCLC).

2019

Recently, immunotherapy has been shown to be an effective and helpful therapeutic option for the treatment of advanced non-small-cell lung cancer (NSCLC). The activity of antitumor T cells may be restored through the checkpoint blockade using anti-programmed death 1 or anti-programmed death ligand 1 (PD-L1) antibodies, showing, in several cancer patients, an increased progression-free survival and overall survival compared with classical chemotherapy. As recently shown by several studies, the PD-L1 expression levels in tumors may offer a selection criterion for patients to predict their immunotherapy response. In particular, NSCLC patients with high tumor PD-L1 levels (proportional score ≥ …

OncologyMalePD-L1030213 general clinical medicinemedicine.medical_specialtyLung Neoplasmsmedicine.medical_treatmentT-LymphocytesProgrammed Cell Death 1 Receptornon-small cell lung cancer (NSCLC)PembrolizumabReviewAntibodies Monoclonal HumanizedNSCLCB7-H1 Antigen03 medical and health sciences0302 clinical medicineAntineoplastic Agents ImmunologicalCheckpoint inhibitorPD-L1Internal medicineCarcinoma Non-Small-Cell LungPD-1medicineHumansPharmacology (medical)Molecular Targeted TherapyLung cancerNeoplasm StagingChemotherapybiologybusiness.industryCancerGeneral MedicineImmunotherapymedicine.diseasePrognosisImmunohistochemistrySurvival AnalysisPredictive biomarker030220 oncology & carcinogenesisbiology.proteinBiomarker (medicine)Lung cancerbusinessPembrolizumabBiomarkersCheckpoint inhibitorsAdvances in therapy
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Characterization of PD-1 and PD-L1 Expression in Papillary Renal Cell Carcinoma: Results of a Large Multicenter Study

2021

Abstract Background Programmed cell death protein 1 (PD-1)/programmed death-ligand 1 (PD-L1) play a decisive role as prognostic markers in clear-cell renal cell carcinoma (RCC). To date, the role of PD-1/PD-L1 as a prognostic marker in papillary RCC (pRCC) remains scarce. Patients and Methods Patients’ sample collection was a joint collaboration of the nationwide PANZAR consortium – a multicenter study. Medical history and tumor specimens were collected from 245 and 129 patients with pRCC types 1 and 2, respectively. Expression of PD-1 and PD-L1 was determined by immunohistochemistry in pRCC and tumor-infiltrating mononuclear cells. Results Of 374 pRCC specimens, 204 type 1 and 97 type 2 we…

Oncologymedicine.medical_specialtyUrologyProgrammed Cell Death 1 Receptor030232 urology & nephrology610DiseaseB7-H1 Antigen03 medical and health sciences0302 clinical medicineRenal cell carcinomaInternal medicinePD-L1Biomarkers TumormedicineHumansMedical historyCarcinoma Renal CellPapillary renal cell carcinomasbiologybusiness.industryPrognosismedicine.diseaseKidney NeoplasmsOncology030220 oncology & carcinogenesisCohortbiology.proteinImmunohistochemistrySample collectionbusinessClinical Genitourinary Cancer
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Endoplasmic Reticulum Stress Inhibition Protects against Excitotoxic Neuronal Injury in the Rat Brain

2007

Elevated brain glutamate with activation of neuronal glutamate receptors accompanies neurological disorders, such as epilepsy and brain trauma. However, the mechanisms by which excitotoxicity triggers neuronal injury are not fully understood. We have studied the glutamate receptor agonist kainic acid (KA) inducing seizures and excitotoxic cell death. KA caused the disintegration of the endoplasmic reticulum (ER) membrane in hippocampal neurons and ER stress with the activation of the ER proteins Bip, Chop, and caspase-12. Salubrinal, inhibiting eIF2α (eukaryotic translation initiation factor 2 subunit α) dephosphorylation, significantly reduced KA-induced ER stress and neuronal deathin vivo…

PERKMaleKainic acidProgrammed cell deathcaspase-12ExcitotoxicityBiologymedicine.disease_causeEndoplasmic ReticulumHippocampusCalcium in biologyeIF2 alphaSalubrinalchemistry.chemical_compoundsalubrinalmedicineExcitatory Amino Acid AgonistsAnimalsRats WistarNeuronsKainic AcidhippocampuGeneral NeuroscienceEndoplasmic reticulumGlutamate receptorBrainNeural InhibitionArticlesCell biologyRatsOxidative StresschemistryUnfolded protein responseNeuroscience
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Neuroglobin and cytoglobin overexpression protects human SH-SY5Y neuroblastoma cells against oxidative stress-induced cell death

2006

Although reactive oxygen species (ROS) at physiological concentrations are required for normal cell function, excessive production of ROS is detrimental to cells. Neuroglobin and cytoglobin are two globins, whose functions are still a matter of debate. A potential role in the detoxification of ROS is suggested. The influence of neuroglobin and cytoglobin on cell death after oxidative stress in human neuroblastoma SH-SY5Y cells was evaluated. Exposure of SH-SY5Y cells to paraquat or H(2)O(2) resulted in a concentration- and time-dependent induction of apoptotic and necrotic cell death. H(2)O(2) was 16 times more potent to induce cell death as compared to paraquat. SH-SY5Y cells transfected w…

ParaquatProgrammed cell deathTime FactorsBlotting WesternGene ExpressionNeuroglobinNerve Tissue ProteinsBiologymedicine.disease_causeNeuroblastomaCell Line TumormedicineHumansGlobinCell DeathDose-Response Relationship DrugHerbicidesGeneral NeuroscienceCytoglobinCytoglobinHydrogen PeroxideTransfectionFlow CytometryOxidantsMolecular biologyGlobinsOxidative StressApoptosisCell cultureNeuroglobinOxidative stressNeuroscience letters
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“Super p53” Mice Display Retinal Astroglial Changes

2013

Tumour-suppressor genes, such as the p53 gene, produce proteins that inhibit cell division under adverse conditions, as in the case of DNA damage, radiation, hypoxia, or oxidative stress (OS). The p53 gene can arrest proliferation and trigger death by apoptosis subsequent to several factors. In astrocytes, p53 promotes cell-cycle arrest and is involved in oxidative stress-mediated astrocyte cell death. Increasingly, astrocytic p53 is proving fundamental in orchestrating neurodegenerative disease pathogenesis. In terms of ocular disease, p53 may play a role in hypoxia due to ischaemia and may be involved in the retinal response to oxidative stress (OS). We studied the influence of the p53 ge…

PathologyAnatomy and PhysiologyCell divisionMouselcsh:MedicineFluorescent Antibody Techniquemedicine.disease_causechemistry.chemical_compoundMiceMolecular Cell Biologylcsh:ScienceMultidisciplinaryGlial fibrillary acidic proteinAnimal ModelsCell biologymedicine.anatomical_structureMedicineOftalmologíaDNA modificationAstrocyteResearch ArticleSignal TransductionProgrammed cell deathmedicine.medical_specialtyCell PhysiologyHistologyOcular AnatomyNeurocienciasMice TransgenicBiologyRetinaModel OrganismsOcular SystemGlial Fibrillary Acidic ProteinmedicineGeneticsAnimalsBiologyRetinaStaining and Labelinglcsh:RRetinalAnatomía ocularMice Inbred C57BLGenética médicaOphthalmologychemistryApoptosisAstrocytesbiology.proteinlcsh:QGene expressionGene FunctionTumor Suppressor Protein p53Animal GeneticsOxidative stress
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Neuronal and BBB damage induced by sera from patients with secondary progressive multiple sclerosis.

2009

An important component of the pathogenic process of multiple sclerosis (MS) is the blood-brain barrier (BBB) damage. We recently set an in vitro model of BBB, based on a three-cell-type co-culture system, in which rat neurons and astrocytes synergistically induce brain capillary endothelial cells to form a monolayer with permeability properties resembling those of the physiological BBB. Herein we report that the serum from patients with secondary progressive multiple sclerosis (SPMS) has a damaging effect on isolated neurons. This finding suggests that neuronal damaging in MS could be a primary event and not only secondary to myelin damage, as generally assumed. SPMS serum affects the perme…

Pathologymedicine.medical_specialtyProgrammed cell deathBlotting WesternBiologyImmunofluorescenceOccludinModels BiologicalMyelinWestern blotOccludinGeneticsmedicineElectric ImpedanceAnimalsmultiple sclerosis brain cell cultures in vitro models of blood-brain barrier neuronal cell death transendothelial electrical resistanceMicroscopy Phase-ContrastRats WistarCells CulturedNeuronsmedicine.diagnostic_testTight junctionCell DeathMultiple sclerosisMembrane ProteinsGeneral MedicineMultiple Sclerosis Chronic Progressivemedicine.diseaseImmunohistochemistryRatsBlotmedicine.anatomical_structurenervous systemBlood-Brain BarrierAstrocytescardiovascular systemInternational journal of molecular medicine
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Comparative study of T84 and T84SF human colon carcinoma cells: in vitro and in vivo ultrastructural and functional characterization of cell culture …

2005

To better understand the relationship between tumor heterogeneity, differentiation, and metastasis, suitable experimental models permitting in vitro and in vivo studies are necessary. A new variant cell line (T84SF) exhibiting an altered phenotype was recently selected from a colon cancer cell line (T84) by repetitive plating on TNF-alpha treated human endothelial cells and subsequent selection for adherent cells. The matched pair of cell lines provides a useful system to investigate the extravasation step of the metastatic cascade. Since analysis of morphological differences can be instructive to the understanding of metastatic potential of tumor cells, we compared the ultrastructural and …

Pathologymedicine.medical_specialtyProgrammed cell deathColon carcinoma ; Tumor cells;. Ultrastructure ; Metastasis .;Apoptosis . ;Bcl-XL;Bcl-XLbcl-X ProteinColon carcinomaApoptosis. UltrastructureBiologyAdenocarcinomaMetastasis .Pathology and Forensic MedicineMetastasischemistry.chemical_compoundMicroscopy Electron TransmissionIn vivoCell Line TumorTumor cellmedicineBiomarkers TumorHumansNeoplasm MetastasisMolecular BiologyCell NucleusCytoplasmic VesiclesTyrosine phosphorylationCell BiologyGeneral Medicinemedicine.diseaseApoptosis .In vitroPhenotypechemistryPleomorphism (cytology)ApoptosisCell cultureGelatinasesColonic NeoplasmsCancer researchDisease ProgressionSignal Transduction
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Neuroprotective effect of flupirtine in prion disease

2003

Apoptotic neuronal cell death is a hallmark of prion diseases. The apoptotic process in neuronal cells is thought to be caused by the scrapie prion protein, PrPSc, and can be experimentally induced by its peptide fragment, PrP106-126. This process is a target for potential drugs to combat prion disease or to ameliorate its symptoms. Flupirtine (Katadolon), a pyridine derivative that is in clinical use as a nonopioid analgesic, has a potent cytoprotective effect, at concentrations above 1 microg/mL, on neuronal cells treated with PrP(Sc) or PrP106-126. This drug acts as an N-methyl-D-aspartate (NMDA) antagonist, but does not bind to NMDA receptors. Flupirtine normalizes the level of intracel…

Pathologymedicine.medical_specialtyProgrammed cell deathanimal diseasesAnalgesicAminopyridinesScrapiePharmacologyNeuroprotectionPrion DiseasesmedicineAnimalsHumansPharmacology (medical)Pharmacologybusiness.industryAntagonistGeneral MedicineGlutathioneGenes bcl-2nervous system diseasesNeuroprotective Agentsnervous systemApoptosisNMDA receptorCalciumFlupirtinebusinessmedicine.drugDrugs of Today
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Synthesis and photocytotoxic activity of [1,2,3]triazolo[4,5-h][1,6]naphthyridines and [1,3]oxazolo[5,4-h][1,6]naphthyridines

2018

Abstract [1,2,3]Triazolo[4,5-h][1,6]naphthyridines and [1,3]oxazolo[5,4-h][1,6]naphthyridines were synthesized with the aim to investigate their photocytotoxic activity. Upon irradiation, oxazolo-naphtapyridines induced light-dependent cell death at nanomolar/low micromolar concentrations (EC50 0.01–6.59 μM). The most photocytotoxic derivative showed very high selectivity and photocytotoxicity indexes (SI = 72–86, PTI>5000), along with a triplet excited state with exceptionally long lifetime (18.0 μs) and high molar absorptivity (29781 ± 180 M−1cm−1 at λmax 315 nm). The light-induced production of ROS promptly induced an unquenchable apoptotic process selectively in tumor cells, with mitoch…

Pharmaceutical ScienceApoptosisMitochondrionPhotochemiotherapy; Photosensitizing agents; Reactive oxygen species; [123]Triazolo[45-h][16]naphthyridines; [13]oxazolo[54-h][16]naphthyridines; Pharmacology; Drug Discovery; Pharmaceutical Science; Organic Chemistry01 natural sciencesMedicinal chemistry[13]oxazolo[54-h][16]naphthyridinechemistry.chemical_compoundDrug Discovery6]naphthyridineschemistry.chemical_classification0303 health sciencesTumorPhotosensitizing AgentsCell DeathSinglet OxygenSinglet oxygenPhotochemiotherapy; Photosensitizing agents; Reactive oxygen species; [1; 2; 3]Triazolo[4; 5-h][1; 6]naphthyridines; [1; 3]oxazolo[5; 4-h][1; 6]naphthyridines; Apoptosis; Cell Death; Cell Line; Tumor; Humans; Lysosomes; Mitochondria; Naphthyridines; Photochemotherapy; Photosensitizing Agents; Reactive Oxygen Species; Singlet OxygenGeneral MedicineLysosomeMitochondriaExcited stateReactive oxygen specie5-h][1HumanProgrammed cell death2NaphthyridinePhotochemiotherapy3]Triazolo[4Cell Line03 medical and health sciences4-h][1Cell Line TumorHumansNaphthyridines030304 developmental biologyPharmacologyReactive oxygen speciesPhotosensitizing agent010405 organic chemistryOrganic ChemistryApoptosi0104 chemical sciences3]oxazolo[5chemistryPhotochemotherapyCell cultureApoptosis[123]Triazolo[45-h][16]naphthyridine[1LysosomesReactive Oxygen SpeciesDerivative (chemistry)
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N-acetylglycoside of oleanolic acid (aridanin) displays promising cytotoxicity towards human and animal cancer cells, inducing apoptotic, ferroptotic…

2020

Abstract Background The discovery of novel phytochemicals represents a reasonable approach to fight malignancies, especially those which are resistant to standard chemotherapy. Purpose We evaluated the cytotoxic potential of a naturally occurring N-acetylglycoside of oleanolic acid, aridanin, on 18 cancer cell lines, including sensitive and drug-resistant phenotypes mediated by P-glycoprotein, BCRP, p53 knockout, deletion-mutated EGFR, or BRAF mutations. Furthermore, metastasizing B16/F10 cells, HepG2 hepatocarcinoma and normal AML12 hepatocytes were investigated. The mechanisms of aridanin-induced cell death was further investigated. Methods The resazurin reduction assay (RRA) was applied …

Pharmacology0303 health sciencesProgrammed cell deathbiologyChemistryNecroptosisPharmaceutical ScienceCell cycle03 medical and health sciences0302 clinical medicineComplementary and alternative medicineApoptosis030220 oncology & carcinogenesisDrug DiscoveryCancer cellbiology.proteinCancer researchMolecular MedicineCytotoxic T cellCytotoxicityCaspase030304 developmental biologyPhytomedicine
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