Search results for "checkpoint"

showing 10 items of 311 documents

Proliferation of aneuploid cells induced by CENP-E depletion is counteracted by the p14ARF tumor suppressor

2018

The spindle assembly checkpoint (SAC) is a cellular surveillance mechanism that ensures the fidelity of chromosomes segregation. Reduced expression of some of its components weakens the SAC and induces chromosome instability and aneuploidy, which are both well-known hallmarks of cancer cells. Centromere protein-E (CENP-E) is a crucial component of the SAC and its function is to facilitate kinetochore microtubule attachment required to achieve and maintain chromosome alignment. The present study investigates the possible role of p14ARF as a controller of aneuploid cells proliferation. We used RNA interference to induce aneuploidy by partial depletion of CENP-E in human primary fibroblasts (I…

0106 biological sciences0301 basic medicineCellAneuploidyHCT116 cellBiologyP14ARF01 natural sciences03 medical and health sciencesp14arfChromosome instabilityCentromereGeneticsmedicineMolecular BiologyChromosomeGeneral MedicineAneuploidymedicine.diseaseCell biologySettore BIO/18 - GeneticaSpindle checkpoint030104 developmental biologymedicine.anatomical_structureRNAiCancer cellCENP-E010606 plant biology & botanyMolecular Genetics and Genomics
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Purine auxotrophy: Possible applications beyond genetic marker

2019

Exploring new drug candidates or drug targets against many illnesses is necessary as "traditional" treatments lose their effectivity. Cancer and sicknesses caused by protozoan parasites are among these diseases. Cell purine metabolism is an important drug target. Theoretically, inhibiting purine metabolism could stop the proliferation of unwanted cells. Purine metabolism is similar across all eukaryotes. However, some medically important organisms or cell lines rely on their host purine metabolism. Protozoans causing malaria, leishmaniasis, or toxoplasmosis are purine auxotrophs. Some cancer forms have also lost the ability to synthesize purines de novo. Budding yeast can serve as an effect…

0106 biological sciencesPurineAuxotrophySaccharomyces cerevisiaeBioengineeringSaccharomyces cerevisiaeBiology01 natural sciencesApplied Microbiology and BiotechnologyBiochemistry03 medical and health scienceschemistry.chemical_compoundDrug DevelopmentNeoplasms010608 biotechnologyGeneticsHumansPurine metabolism030304 developmental biology0303 health sciencesAdenineEukaryotaCell Cycle CheckpointsMetabolismCell cyclebiology.organism_classificationYeastchemistryBiochemistryPurinesCancer cellBiotechnologyYeast
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Deduplication Potential of HPC Applications’ Checkpoints

2016

HPC systems contain an increasing number of components, decreasing the mean time between failures. Checkpoint mechanisms help to overcome such failures for long-running applications. A viable solution to remove the resulting pressure from the I/O backends is to deduplicate the checkpoints. However, there is little knowledge about the potential to save I/Os for HPC applications by using deduplication within the checkpointing process. In this paper, we perform a broad study about the deduplication behavior of HPC application checkpointing and its impact on system design.

0301 basic medicine03 medical and health sciences030104 developmental biologyComputer scienceDistributed computingScalabilityData_FILESRedundancy (engineering)Data deduplicationApplication checkpointing2016 IEEE International Conference on Cluster Computing (CLUSTER)
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Rosmarinic Acid Activates AMPK to Inhibit Metastasis of Colorectal Cancer

2018

Rosmarinic acid (RA) has been used as an anti-inflammatory, anti-diabetic, and anti-cancer agent. Although RA has also been shown to exert an anti-metastatic effect, the mechanism of this effect has not been reported to be associated with AMP-activated protein kinase (AMPK). The aim of this study was to elucidate whether RA could inhibit the metastatic properties of colorectal cancer (CRC) cells via the phosphorylation of AMPK. RA inhibited the proliferation of CRC cells through the induction of cell cycle arrest and apoptosis. In several metastatic phenotypes of CRC cells, RA regulated epithelial–mesenchymal transition (EMT) through the upregulation of an epithelial marker, E-cadherin, and…

0301 basic medicineAMPKrosmarinic acidCell cycle checkpointmatrix metalloproteinaseVimentincolorectal cancerMetastasis03 medical and health sciences0302 clinical medicineDownregulation and upregulationmedicinemetastasisPharmacology (medical)Protein kinase AOriginal ResearchPharmacologybiologyChemistryCell adhesion moleculelcsh:RM1-950EMTAMPKmedicine.disease030104 developmental biologylcsh:Therapeutics. PharmacologyApoptosis030220 oncology & carcinogenesisCancer researchbiology.proteinFrontiers in Pharmacology
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Retinoic Acid affects Lung Adenocarcinoma growth by inducing differentiation via GATA6 activation and EGFR and Wnt inhibition

2016

AbstractA fundamental task in cancer research aims at the identification of new pharmacological therapies that can affect tumor growth. Differentiation therapy might exploit this function not only for hematological diseases, such as acute promyelocytic leukemia (APML) but also for epithelial tumors, including lung cancer. Here we show that Retinoic Acid (RA) arrests in vitro and in vivo the growth of Tyrosine Kinase Inhibitors (TKI) resistant Non Small Cell Lung Cancer (NSCLC). In particular, we found that RA induces G0/G1 cell cycle arrest in TKI resistant NSCLC cells and activates terminal differentiation programs by modulating the expression of GATA6, a key transcription factor involved …

0301 basic medicineAcute promyelocytic leukemiaScienceEGFRRetinoic acidMice NudeTretinoinBiologyArticle03 medical and health scienceschemistry.chemical_compoundDifferentiation therapySettore BIO/13 - Biologia ApplicataCarcinoma Non-Small-Cell LungCell Line TumorGATA6 Transcription FactormedicineRetinoic acidAnimalsHumansLung cancerProtein Kinase InhibitorsWnt Signaling PathwayTranscription factorCell ProliferationMultidisciplinaryQRWnt signaling pathwayCell Differentiationmedicine.diseaseG1 Phase Cell Cycle CheckpointsXenograft Model Antitumor Assaysrespiratory tract diseasesErbB Receptorslung cancerAnimals; Carcinoma Non-Small-Cell Lung; Cell Differentiation; Cell Line Tumor; Cell Proliferation; Drug Resistance Neoplasm; ErbB Receptors; G1 Phase Cell Cycle Checkpoints; GATA6 Transcription Factor; Humans; Mice Nude; Protein Kinase Inhibitors; Signal Transduction; Tretinoin; Wnt Signaling Pathway; Xenograft Model Antitumor Assays030104 developmental biologychemistryDrug Resistance NeoplasmImmunologyCancer researchMedicineAdenocarcinomaEngineering sciences. TechnologyTyrosine kinaseSignal Transduction
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Mutanome directed cancer immunotherapy

2015

Somatic mutations are important drivers of cancer development. Accumulating evidence suggests that a significant subset of mutations result in neo-epitopes recognized by autologous T cells and thus may constitute the Achilles' heel of tumor cells. T cells directed against mutations have been shown to have a key role in clinical efficacy of potent cancer immunotherapy modalities, such as adoptive transfer of autologous tumor infiltrating lymphocytes and immune checkpoint inhibitors. Whereas these findings strengthen the idea of a prominent role of neo-epitopes in tumor rejection, the systematic therapeutic exploitation of mutations was hampered until recently by the uniqueness of the reperto…

0301 basic medicineAdoptive cell transferSomatic cellT-Lymphocytesmedicine.medical_treatmentImmune checkpoint inhibitorsImmunology03 medical and health sciences0302 clinical medicineCancer immunotherapyAntigens NeoplasmNeoplasmsAnimalsHumansImmunology and AllergyMedicineClinical efficacybusiness.industryAutologous T-cellsImmune recognition030104 developmental biology030220 oncology & carcinogenesisTumor rejectionMutationImmunologyImmunotherapybusiness
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Cytoprotective and antioxidant properties of organic selenides for the myelin-forming cells, oligodendrocytes.

2018

Abstract Here a new series of twenty-one organoselenides, of potential protective activity, were synthesized and tested for their intrinsic cytotoxicity, anti-apoptotic and antioxidant capacities in oligodendrocytes. Most of the organoselenides were able to decrease the ROS levels, revealing antioxidant properties. Compounds 5b and 7b showed a high glutathione peroxidase (GPx)-like activities, which were 1.5 folds more active than ebselen. Remarkably, compound 5a diminished the formation of the oligodendrocytes SubG1 peak in a concentration-dependent manner, indicating its anti-apoptotic properties. Furthermore, based on the SwissADME web interface, we performed an in-silico structure-activ…

0301 basic medicineAntioxidantCell Survivalmedicine.medical_treatmentMolecular ConformationApoptosisCrystallography X-RayProtective Agents01 natural sciencesBiochemistryAntioxidantsCell Line03 medical and health scienceschemistry.chemical_compoundMyelinMiceStructure-Activity RelationshipOrganoselenium CompoundsDrug DiscoverymedicineAnimalsCytotoxicityMolecular Biologychemistry.chemical_classification010405 organic chemistryEbselenGlutathione peroxidaseOrganic ChemistryNeurodegenerationCells oligodendrocytesmedicine.diseaseG1 Phase Cell Cycle Checkpoints0104 chemical sciencesOligodendroglia030104 developmental biologymedicine.anatomical_structurechemistryBiochemistryApoptosisDrug DesignReactive Oxygen SpeciesBioorganic chemistry
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Trabectedin triggers direct and NK-mediated cytotoxicity in multiple myeloma

2019

Background Genomic instability is a feature of multiple myeloma (MM), and impairment in DNA damaging response (DDR) has an established role in disease pathobiology. Indeed, a deregulation of DNA repair pathways may contribute to genomic instability, to the establishment of drug resistance to genotoxic agents, and to the escape from immune surveillance. On these bases, we evaluated the role of different DDR pathways in MM and investigated, for the first time, the direct and immune-mediated anti-MM activity of the nucleotide excision repair (NER)-dependent agent trabectedin. Methods Gene-expression profiling (GEP) was carried out with HTA2.0 Affymetrix array. Evaluation of apoptosis, cell cyc…

0301 basic medicineCancer ResearchCell cycle checkpointNatural killerDNA repairmedicine.medical_treatmentMyelomalcsh:RC254-28203 medical and health sciences0302 clinical medicineMicro-RNAmedicineHumansMolecular BiologyAntineoplastic Agents AlkylatingTrabectedin3D-modelChemistrylcsh:RC633-647.5ResearchMicro-RNAsHematologylcsh:Diseases of the blood and blood-forming organsCell cycleNKG2Dlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensKiller Cells Natural030104 developmental biologyCytokineOncologyApoptosis3D-models030220 oncology & carcinogenesis3D-models; Micro-RNAs; Myeloma; Natural killer; TrabectedinCancer researchDNA fragmentationMultiple Myelomamedicine.drugTrabectedinJournal of Hematology & Oncology
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Oxidative stress preconditioning of mouse perivascular myogenic progenitors selects a subpopulation of cells with a distinct survival advantage in vi…

2018

AbstractCell engraftment, survival and integration during transplantation procedures represent the crux of cell-based therapies. Thus, there have been many studies focused on improving cell viability upon implantation. We used severe oxidative stress to select for a mouse mesoangioblast subpopulation in vitro and found that this subpopulation retained self-renewal and myogenic differentiation capacities while notably enhancing cell survival, proliferation and migration relative to unselected cells. Additionally, this subpopulation of cells presented different resistance and recovery properties upon oxidative stress treatment, demonstrating select advantages over parental mesoangioblasts in …

0301 basic medicineCancer ResearchCellular differentiationCellstem cells; oxidative stress; clone isolation/dk/atira/pure/subjectarea/asjc/2800/2804Mice SCIDp38 Mitogen-Activated Protein KinasesMiceCell MovementProtein IsoformsMuscular Dystrophy/dk/atira/pure/subjectarea/asjc/2400/2403Settore BIO/06 - Anatomia Comparata E Citologiaeducation.field_of_studylcsh:CytologyStem CellsSettore BIO/13Cell DifferentiationSkeletalCell biologymedicine.anatomical_structureMuscleMatrix Metalloproteinase 2Animals; Cell Cycle Checkpoints; Cell Differentiation; Cell Line; Cell Movement; Cell Survival; Hydrogen Peroxide; Matrix Metalloproteinase 2; Mice; Mice SCID; Muscle Skeletal; Muscular Dystrophy Animal; Oxidative Stress; Protein Isoforms; Reactive Oxygen Species; Sarcoglycans; Stem Cell Transplantation; Stem Cells; p38 Mitogen-Activated Protein Kinases/dk/atira/pure/subjectarea/asjc/1300/1306/dk/atira/pure/subjectarea/asjc/1300/1307Cell SurvivalPopulationImmunologyBiologySCIDArticleCell Line03 medical and health sciencesCellular and Molecular NeuroscienceIn vivoSarcoglycansmedicineAnimalsProgenitor celllcsh:QH573-671educationMuscle Skeletaloxidative streMesoangioblastAnimalCell BiologyCell Cycle CheckpointsHydrogen PeroxideMuscular Dystrophy Animalclone isolationTransplantationstem cellOxidative Stress030104 developmental biologyCell cultureReactive Oxygen SpeciesStem Cell TransplantationCell Death & Disease
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Tumour mutational burden as a biomarker for immunotherapy: Current data and emerging concepts

2020

International audience; Treatment with immune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) or its ligand (PD-L1) can generate durable responses in various cancer types, but only in a subset of patients. The use of predictive biomarkers for response to PD-1/PD-L1 inhibitors is critical for patient selection. Expression of PD-L1 has demonstrated utility in patient selection. Tumour mutational burden (TMB) is an emerging biomarker for response to PD-1/PD-L1 inhibitors. The evaluation of this biomarker is based on the hypothesis that a high number of mutations in somatic exonic regions will lead to an increase in neoantigen production, which could then be recognised by…

0301 basic medicineCancer ResearchImmune checkpoint inhibitorsmedicine.medical_treatment[SDV]Life Sciences [q-bio]DNA Mutational AnalysisProgrammed Cell Death 1 ReceptorTumour mutational burdenBioinformaticsArticleB7-H1 Antigen03 medical and health sciencesAntineoplastic Agents Immunological0302 clinical medicineImmune systemNeoplasmsBiomarkers TumorHumansMedicineIn patientGenetic TestingPredictive biomarkerbusiness.industryPatient SelectionCancerBiomarkerImmunotherapymedicine.disease3. Good healthBiomarker (cell)[SDV] Life Sciences [q-bio]030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisMutationImmunotherapybusinessCD8
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