Search results for "programme"

showing 10 items of 874 documents

Activated kRas protects colon cancer cells from cucurbitacin-induced apoptosis: The role of p53 and p21

2008

Cucurbitacins have been shown to inhibit proliferation in a variety of cancer cell lines. The aim of this study was to determine their biological activity in colon cancer cell lines that do not harbor activated STAT3, the key target of cucurbitacin. In order to establish the role of activated kRas in the responsiveness of cells to cucurbitacins, we performed experiments in isogenic colon cancer cell lines, HCT116 and Hke-3, which differ only by the presence of an activated kRas allele. We compared the activity of 23, 24-dihydrocucurbitacin B (DHCB) and cucurbitacin R (CCR), two cucurbitacins that we recently isolated, with cucurbitacin I (CCI), a cucurbitacin with established antitumorigeni…

Cyclin-Dependent Kinase Inhibitor p21Programmed cell deathTumor suppressor geneAntineoplastic AgentsApoptosisBiologymedicine.disease_causeBiochemistryArticleProto-Oncogene Proteins p21(ras)CucurbitacinsCell Line TumorProto-Oncogene ProteinsmedicineHumansCell ProliferationPharmacologyCell growthCucurbitacinTriterpenesdigestive system diseasesCell cultureApoptosisColonic Neoplasmsras ProteinsCancer researchKRASTumor Suppressor Protein p53Biochemical Pharmacology
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The role of reactive oxygen species and subsequent DNA-damage response in the emergence of resistance towards resveratrol in colon cancer models

2014

AbstractIn spite of the novel strategies to treat colon cancer, mortality rates associated with this disease remain consistently high. Tumour recurrence has been linked to the induction of resistance towards chemotherapy that involves cellular events that enable cancer cells to escape cell death. Treatment of colon cancer mainly implicates direct or indirect DNA-damaging agents and increased repair or tolerances towards subsequent lesions contribute to generate resistant populations. Resveratrol (RSV), a potent chemosensitising polyphenol, might share common properties with chemotherapeutic drugs through its indirect DNA-damaging effects reported in vitro. In this study, we investigated how…

Cyclin-Dependent Kinase Inhibitor p21SenescenceCancer ResearchProgrammed cell deathColonDNA damageColorectal cancerImmunologyApoptosisBiologyResveratrolS PhaseHistonesPolyploidyCellular and Molecular Neurosciencechemistry.chemical_compoundCell Line TumorStilbenesmedicineAnimalsHumansCHEK1Cyclin-Dependent Kinase Inhibitor p16Cell Biologymedicine.diseaseAntineoplastic Agents PhytogenicRatsGene Expression Regulation NeoplasticCheckpoint Kinase 2chemistryDrug Resistance NeoplasmResveratrolApoptosisCheckpoint Kinase 1Cancer cellImmunologyCancer researchOriginal ArticleTumor Suppressor Protein p53Reactive Oxygen SpeciesProtein KinasesDNA DamageSignal TransductionCell Death & Disease
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Dynamic intracellular survivin in oral squamous cell carcinoma: underlying molecular mechanism and potential as an early prognostic marker

2007

Survivin functions as an apoptosis inhibitor and a regulator of cell division in many tumours. The intracellular localization of survivin in tumours has been suggested as a prognostic marker. However, current reports are inconsistent and the underlying molecular mechanisms are not understood. The present study has examined the localization and prognostic value of nuclear and cytoplasmic survivin in the pre-therapeutic biopsies from 71 oral and oropharyngeal squamous carcinoma (OSCC) patients. Statistical analysis indicated that preferential nuclear versus cytoplasmic survivin correlated with favourable versus unfavourable disease outcome. Uni- and multi-variate analysis showed that in contr…

CytoplasmProgrammed cell deathPathologymedicine.medical_specialtySurvivinReceptors Cytoplasmic and NuclearApoptosisKaplan-Meier EstimateCysteine Proteinase InhibitorsKaryopherinsInhibitor of Apoptosis ProteinsPathology and Forensic MedicineCell Line TumorSurvivinBiomarkers TumorCarcinomaHumansMedicineNuclear export signalneoplasmsCell NucleusNuclear Export SignalsPredictive markerbusiness.industryCell cyclePrognosismedicine.diseaseImmunohistochemistryNeoplasm ProteinsSquamous carcinomaOropharyngeal NeoplasmsHead and Neck NeoplasmsApoptosisCarcinoma Squamous CellCancer researchMouth NeoplasmsbusinessMicrotubule-Associated ProteinsThe Journal of Pathology
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How DNA lesions are turned into powerful killing structures: Insights from UV-induced apoptosis

2008

Mammalian cells treated with ultraviolet (UV) light provide one of the best-known experimental systems for depicting the biological consequences of DNA damage. UV irradiation induces the formation of DNA photoproducts, mainly cyclobutane pyrimidine dimers (CPDs) and (6-4) pyrimidine-pyrimidone photoproducts [(6-4)PPs], that drastically impairs DNA metabolism, culminating in the induction of cell death by apoptosis. While CPDs are the most important apoptosis-inducing lesions in DNA repair proficient cells, recent data indicates that (6-4)PPs also signals for apoptosis in DNA repair deficient cells. The toxic effects of these unrepaired DNA lesions are commonly associated with transcription …

DNA ReplicationMAPK/ERK pathwayProgrammed cell deathBase SequenceTranscription GeneticUltraviolet RaysDNA repairDNA damageHealth Toxicology and MutagenesisMolecular Sequence DataApoptosisPyrimidine dimerBiologyCell biologychemistry.chemical_compoundchemistryBiochemistryApoptosisAutophagyGeneticsUltraviolet lightAnimalsHumansDNADNA DamageMutation Research/Reviews in Mutation Research
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The APC/C cofactor Cdh1 prevents replicative stress and p53-dependent cell death in neural progenitors

2013

The E3-ubiquitin ligase APC/C-Cdh1 is essential for endoreduplication but its relevance in the mammalian mitotic cell cycle is still unclear. Here we show that genetic ablation of Cdh1 in the developing nervous system results in hypoplastic brain and hydrocephalus. These defects correlate with enhanced levels of Cdh1 substrates and increased entry into the S phase in neural progenitors. However, cell division is prevented in the absence of Cdh1 due to hyperactivation of cyclin-dependent kinases, replicative stress, induction of p53, G2 arrest and apoptotic death of these progenitor cells. Concomitant ablation of p53 rescues apoptosis but not replicative stress, resulting in the presence of …

DNA ReplicationMaleProgrammed cell deathCell divisionNeurogenesisGeneral Physics and AstronomyApoptosisCell Cycle ProteinsBiologyAnaphase-Promoting Complex-CyclosomeCdh1 ProteinsGeneral Biochemistry Genetics and Molecular BiologyMice03 medical and health sciences0302 clinical medicineNeural Stem CellsAnimalsProgenitor cell030304 developmental biologyProgenitorMice KnockoutNeuronschemistry.chemical_classification0303 health sciencesDNA ligaseMultidisciplinaryCell CycleNeurogenesisBrainOrgan SizeGeneral ChemistryCell cycle3. Good healthCell biologyMice Inbred C57BLchemistrySynaptic plasticityFemaleTumor Suppressor Protein p53Cell Division030217 neurology & neurosurgeryNature Communications
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Processing of O6-methylguanine into DNA double-strand breaks requires two rounds of replication whereas apoptosis is also induced in subsequent cell …

2009

The DNA adduct O(6)-methylguanine (O(6)MeG) induced by environmental genotoxins and anticancer drugs is a highly mutagenic, genotoxic and apoptotic lesion. Apoptosis induced by O(6)MeG requires mismatch repair (MMR) and proliferation. Models of O(6)MeG-triggered cell death postulate that O(6)MeG/T mispairs activate MMR giving rise to either direct genotoxic signaling or secondary lesions that trigger apoptotic signaling in the 2(nd) replication cycle. To test these hypotheses, we used a highly synchronized cell system competent and deficient for the repair of O(6)MeG adducts, which were induced by the S(N)1 methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). We show that DNA doub…

DNA ReplicationProgrammed cell deathMethylnitronitrosoguanidineCell cycle checkpointGuanineDNA repairBlotting WesternSuccinimidesApoptosisCHO CellsBiologychemistry.chemical_compoundO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeDNA adductAnimalsDNA Breaks Double-StrandedMolecular BiologyCell CycleCell BiologyCell cycleFlow CytometryFluoresceinsMolecular biologyCell biologychemistryMicroscopy FluorescenceApoptosisDNA mismatch repairDNADevelopmental BiologyCell cycle (Georgetown, Tex.)
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Apoptotic death induced by the cyclophosphamide analogue mafosfamide in human lymphoblastoid cells: Contribution of DNA replication, transcription in…

2007

Cyclophosphamide is one of the most often used anticancer drugs. Although DNA interstrand cross-links are considered responsible for its cytotoxicity, the mechanism of initiation and execution of cell death is largely unknown. Using the cyclophosphamide analogue mafosfamide, which does not need metabolic activation, we show that mafosfamide induces apoptosis dose and time dependently in lymphoblastoid cells, with clearly more apoptosis in p53(wt) cells. We identified two upstream processes that initiate apoptosis, DNA replication blockage and transcriptional inhibition. In lymphoblastoid cells, wherein DNA replication can be switched off by tetracycline, proliferation is required for induci…

DNA ReplicationProgrammed cell deathTime FactorsTranscription GeneticDNA damageDrug ResistanceAntineoplastic AgentsApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein Serine-Threonine KinasesToxicologyCaspase-Dependent ApoptosisCell Linechemistry.chemical_compoundMafosfamideHumansCHEK1PhosphorylationCyclophosphamideCaspaseCell ProliferationPharmacologyDose-Response Relationship DrugbiologyTumor Suppressor ProteinsCell cycleDNA-Binding ProteinsCheckpoint Kinase 2chemistryApoptosisCaspasesCheckpoint Kinase 1Cancer researchbiology.proteinTumor Suppressor Protein p53Protein KinasesSignal TransductionToxicology and Applied Pharmacology
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The histone deacetylase inhibitor suberoylanilide hydroxamic acid sensitizes human hepatocellular carcinoma cells to TRAIL-induced apoptosis by TRAIL…

2009

Abstract This paper shows that the histone deacetylase inhibitor SAHA sensitised at sub-toxic doses human hepatocellular carcinoma cells (HepG2, Hep3B and SK-Hep1) to TRAIL-induced apoptosis, while it was ineffective in primary human hepatocytes (PHHs). In particular in HCC cells SAHA increased the expression of death receptor 5 (DR5) and caused a decrement of c-Flip. These two modifications provoked in the presence of TRAIL the rapid production of TRAIL-DISC and the activation of caspase-8. Consequently SAHA/TRAIL combination induced many apoptotic events, such as a cleavage of Bid into tBid, dissipation of mitochondrial membrane potential, activation of caspase-3 with the consequent cleav…

Death Domain Receptor Signaling Adaptor ProteinsCancer Researchmedicine.medical_specialtyProgrammed cell deathCarcinoma Hepatocellularmedicine.drug_classmedicine.medical_treatmentBlotting WesternCASP8 and FADD-Like Apoptosis Regulating ProteinDown-RegulationAntineoplastic AgentsApoptosisBiologyHydroxamic AcidsHDACI TRAIL apoptosisInternal medicineSettore BIO/10 - BiochimicamedicineHumansProtein kinase BVorinostatLiver NeoplasmsHistone deacetylase inhibitorNF-kappa Bmedicine.diseaseReceptors TNF-Related Apoptosis-Inducing LigandCytokineEndocrinologyOncologyDrug Resistance NeoplasmApoptosisHepatocellular carcinomaCancer researchTumor necrosis factor alphaSignal transductionProto-Oncogene Proteins c-akt
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Pedagogika społeczna jako oferta studiów magisterskich w powojennej Polsce (1945-1949)

2021

The article presents graduate programs (Masters level) in the field of social pedagogy off ered by Helena Radlińska and her colleagues at the University of Łódź aft er WWII. Socio-Pedagogical studies established at the Department of Social Pedagogy at the University of Łódz were supposed to prepare educational, social, and cultural workers in time of revival of Poland after 1945. Th e example of the educational model created at that time can serve as an inspiration in the development of contemporary programs of education rooted in the Polish socio-pedagogical tradition

Department of Social Pedagogy of the University of ŁódzHelena RadlińskaMA programme in social pedagogysocial pedagogyStudia z Teorii Wychowania
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Mentor – A Trustee for Disadvantaged Youth

2015

<p><em><span lang="EN-GB">The perception of oneself and the surrounding environment are developed during childhood. The behaviour of others directly influences the attitude towards oneself and decisions and observations about one`s value. One of the biggest deficiencies of institutional out-of-family care that significantly hinders the comprehensive development of children is the inability of children to form close bonds with adults. To come to a conclusion that you are not loved and worthless means the feel of deep disappointment. The child becomes shore that he has been deceived and abandoned. These thoughts evoke protests, depression, and insecurity. Due to these miscon…

DisappointmentEmotional supportSocioemotional selectivity theorymedia_common.quotation_subjecteducationmentor; mentee; mentor programme; young adultYouth mentoringhumanitiesDisadvantagedDevelopmental psychologyPerceptionmedicinemedicine.symptomPsychologySocial psychologymedia_commonSOCIETY. INTEGRATION. EDUCATION. Proceedings of the International Scientific Conference
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