Search results for "antineoplastic"

showing 10 items of 2217 documents

“Mitotic Slippage” and Extranuclear DNA in Cancer Chemoresistance: A Focus on Telomeres

2020

Mitotic slippage (MS), the incomplete mitosis that results in a doubled genome in interphase, is a typical response of TP53-mutant tumors resistant to genotoxic therapy. These polyploidized cells display premature senescence and sort the damaged DNA into the cytoplasm. In this study, we explored MS in the MDA-MB-231 cell line treated with doxorubicin (DOX). We found selective release into the cytoplasm of telomere fragments enriched in telomerase reverse transcriptase (hTERT), telomere capping protein TRF2, and DNA double-strand breaks marked by γH2AX, in association with ubiquitin-binding protein SQSTM1/p62. This occurs along with the alternative lengthening of telomeres (ALT) and DNA repa…

PolyploidizationALTSQSTM1/p62lcsh:ChemistryNeoplasmsSequestosome-1 Proteincellular senescenceTelomeric Repeat Binding Protein 2mtTP53 cancerTelomeraseAmoeboid conversionlcsh:QH301-705.5Telomere ShorteningSpectroscopyAntibiotics AntineoplasticGeneral MedicineTelomereComputer Science ApplicationsCell biologyinverted meiosisExtranuclear DNA<i>mtTP53</i> cancerSpo11DNA repairTelomere CappingMitosisBudding of mitotic progenygenotoxic treatmentamoeboid conversionInverted meiosisBiologyCellular senescenceArticleCatalysisInorganic ChemistryMeiosisCell Line Tumorextranuclear DNAHumansTelomerase reverse transcriptasePhysical and Theoretical ChemistryMolecular BiologyMitosisCell ProliferationGenotoxic treatmentOrganic ChemistryRecombinational DNA RepairCell Cycle CheckpointsDNA<i>SQSTM1/p62</i>polyploidizationTelomerelcsh:Biology (General)lcsh:QD1-999DoxorubicinDrug Resistance Neoplasmbiology.proteinHomologous recombinationbudding of mitotic progenyDNA DamageInternational Journal of Molecular Sciences
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Polypoid anal melanoma. A case report and review of the literature

2016

Ano-rectal melanoma is an uncommon finding in patients complaining of rectal bleeding and/or anal mass often misinterpreted as a haemorroidal pile.A 55-years-old woman, complaining of rectal bleeding, frequent anal pain and anal mass suspected for haemorroidal thrombosis was referred for evaluation and possible treatment. A brown polypoid mass arising from the anal canal/lower rectum with a maximum diameter of 6 cm was diagnosed. The hystological examination of the neoplasm, transanally removed, revealed the presence of a polypoid melanoma partially involving the resection margin. Nor metastases nor limph-node involvement were found at the total-body CT scan and at a CT-PET. C-KIT examinati…

PrognosiHemorrhoidsDiagnosis DifferentialTreatment RefusalAnus NeoplasmAntineoplastic Combined Chemotherapy ProtocolsHumansmucosal melanomaNeoplasm Invasivenessrectal bleedingMelanomaDigestive System Surgical ProceduresNeoplasm InvasiveneAntineoplastic Combined Chemotherapy Protocolano-rectal melanoma; mucosal melanoma; rectal bleedingRectal DiseaseDigestive System Surgical ProcedureMiddle AgedAnus NeoplasmsPrognosisRectal DiseasesChemotherapy Adjuvantano-rectal melanomaFemaleHemorrhoidGastrointestinal HemorrhageHuman
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Tributyltin(IV) ferulate, a novel synthetic ferulic acid derivative, induces autophagic cell death in colon cancer cells: From chemical synthesis to …

2020

Ferulic acid (FA) is a natural phenolic phytochemical that has low toxicity and exhibits therapeutic effects against various diseases, behaving as an antioxidant. FA also displays modest antitumor properties that have been reported at relatively high concentrations. With the aim of improving the anti-tumor efficacy of FA, we synthesized the novel compound tributyltin(IV) ferulate (TBT-F). The coordination environment at the tin center was investigated spectroscopically. Following synthesis, chemical characterization and computational analysis, we evaluated TBT-F effects in colon cancer cells. The results showed that TBT-F, at nanomolar range concentrations, was capable of reducing the viabi…

Programmed cell deathAntioxidantCoumaric AcidsAutophagic Cell Deathmedicine.medical_treatmentAntineoplastic AgentsOrganotin(IV)VacuolePharmacology010402 general chemistry01 natural sciencesBiochemistryInorganic ChemistryFerulic acidchemistry.chemical_compoundColon cancer cytotoxicityLC3medicineHumansViability assay010405 organic chemistryChemistryp62AutophagyFerulic acidHCT116 Cells0104 chemical sciencesApoptosisCell Death ProcessColonic NeoplasmsCaco-2 CellsTrialkyltin CompoundsHT29 CellsJournal of Inorganic Biochemistry
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Cytotoxicity and apoptosis induction by Fumaria officinalis extracts in leukemia and multiple myeloma cell lines

2021

Abstract Ethnopharmacological relevance Fumaria officinalis (Fumariaceae) is recorded in the Kurdish ethnobotany for various health problems. Aim of the study: In this study, the cytotoxic activity of F. officinalis extracts on two leukemia and nine multiple myeloma (MM) cell lines was investigated. Materials and methods: The cytotoxic and ferroptotic activity were examined by resazurin reduction assay. Flow cytometry, immunoblotting assay and fluorescence microscopy were used to measure cell cycle distribution, apoptosis, induction of reactive oxygen species (ROS), loss integrity of mitochondrial membrane potential (MMP) and autophagy. LC-ESI/MS was used to identify chemical constituents p…

Programmed cell deathApoptosisFlow cytometryInhibitory Concentration 5003 medical and health sciences0302 clinical medicineCell Line TumorDrug DiscoveryAutophagymedicineHumansCytotoxicity030304 developmental biologyMembrane Potential MitochondrialPharmacology0303 health sciencesLeukemiamedicine.diagnostic_testbiologyPlant ExtractsChemistryCell growthFumariaFumaria officinalisCell cyclebiology.organism_classificationAntineoplastic Agents PhytogenicMolecular biologyApoptosis030220 oncology & carcinogenesisOfficinalisMultiple MyelomaReactive Oxygen SpeciesJournal of Ethnopharmacology
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Antitumor effects of dehydroxymethylepoxyquinomicin, a novel nuclear factor-kappaB inhibitor, in human liver cancer cells are mediated through a reac…

2009

Activation of the nuclear transcription factor-kappa B (NF-kappa B) has been implicated in liver tumorigenesis. We evaluated the effects of a novel NF-kappa B inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), in two human liver cancer cell lines HA22T/VGH and HuH-6. DHMEQ treatment dose dependently decreased the DNA-binding capacity of the NF-kappa B p65 subunit, inhibited cell growth and proliferation, and increased apoptosis as shown by caspase activation, release of cytochrome c, poly(ADP-ribose) polymerase cleavage, and down-regulation of survivin. DHMEQ also induced a dose-dependent activation of mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling, …

Programmed cell deathCarcinoma HepatocellularBIOLOGICAL-ACTIVITIESDrug Evaluation PreclinicalDown-RegulationAntineoplastic AgentsApoptosisBiologymedicine.disease_causeACTIVATIONchemistry.chemical_compoundHYDROGEN-PEROXIDEENDOPLASMIC-RETICULUM STRESSCell Line TumorSurvivinNADPH OXIDASEmedicineHumansOXIDATIVE STRESSProtein kinase AEndoplasmic Reticulum Chaperone BiPINDUCED APOPTOSISCell ProliferationPharmacologySettore MED/12 - GastroenterologiaDose-Response Relationship DrugUNFOLDED PROTEIN RESPONSECell growthCyclohexanonesINDUCTIONLiver NeoplasmsDEATHNF-kappa BCytochromes cMolecular biologyCell biologyEnzyme ActivationchemistryApoptosisCaspasesCancer cellBenzamidesSettore BIO/14 - FarmacologiaMolecular MedicineGrowth inhibitionMitogen-Activated Protein KinasesPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesOxidative stressMolecular pharmacology
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COX-2-dependent and COX-2-independent mode of action of celecoxib in human liver cancer cells.

2011

Celecoxib (Celebrex((R)), Pfizer) is a selective cyclooxygenase-2 (COX-2) inhibitor with chemopreventive and antitumor effects. However, it is now well known that celecoxib has several COX-2-independent activities. To better understand COX-2-independent molecular mechanisms underlying the antitumor activity of celecoxib, we investigated the expression profile of the celecoxib-treated COX-2-positive (Huh7) and COX-2-negative (HepG2) liver cancer cell lines, using microarray analysis. Celecoxib treatment resulted in significantly altered expression levels of 240 and 403 transcripts in Huh7 and HepG2 cells, respectively. Confirmation of the microarray results was performed for selected genes b…

Programmed cell deathCarcinoma HepatocellularMicroarrayTranscription GeneticHepatocellular carcinomaCell SurvivalAntineoplastic AgentsPharmacologyBiologyBiochemistryCell Line TumorGeneticsmedicineHumansMode of actionneoplasmsMolecular BiologySulfonamidesCyclooxygenase 2 InhibitorsCell growthMicroarray analysis techniquesGene Expression ProfilingLiver NeoplasmsCOX-2Gene expression profilingGene Expression Regulation NeoplasticCell cultureCelecoxibCyclooxygenase 2CelecoxibMolecular MedicinePyrazolesBiotechnologymedicine.drugSignal TransductionOmics : a journal of integrative biology
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Tumor cell specific toxicity of Inula helenium extracts.

2006

The aim of the research program was to identify botanical extracts with antineoplastic activity. In this respect extracts prepared from Inula helenium roots showed a remarkable activity. As evidenced by the MTT assay, the Inula helenium extract revealed a highly selective toxicity toward four different tumor cell lines (HT-29, MCF-7, Capan-2 and G1), but a much lower toxicity against healthy human peripheral blood lymphocytes (PBLs) from two donors. The extract-induced death of tumor cells was studied extensively by electron microscopy. There was a remarkable similarity of morphological alterations observed in the four cell lines: patchy chromatin condensations, cytoplasmic vesiculation, sw…

Programmed cell deathCell SurvivalContext (language use)Plant RootsLethal Dose 50Cell Line TumorToxicity Tests AcuteHumansMTT assayLymphocytesAnnexin A5CytotoxicityPharmacologyInulabiologyMutagenicity TestsPlant Extractsbiology.organism_classificationMolecular biologyAntineoplastic Agents PhytogenicApoptosisCell cultureImmunologyInulaHT29 CellsHeleniumPhytotherapy research : PTR
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Molecular mechanisms of rosmarinic acid from Salvia miltiorrhiza in acute lymphoblastic leukemia cells

2015

Abstract Ethnopharmacological relevance Rosmarinic acid (RA), a major hydrosoluble bioactive compound found in the Chinese medicinal herb, Salvia miltiorrhiza Bunge, which has been used in traditional Chinese medicine to treat various diseases, including cancer. However, the mechanisms have not been fully elucidated. Aim of the study Guided by microarray hybridization and Ingenuity Pathway Analysis, we identified modes of action of rosmarinic acid (RA) isolated from S. miltiorrhiza on acute lymphoblastic leukemia cells. Materials and methods Microarray data were verified by independent methods: Real-time RT-PCR (mRNA expression), resazurin assay (cytotoxicity of RA towards parental CCRF-CEM…

Programmed cell deathCell SurvivalDNA damageNecroptosisCellAntineoplastic AgentsApoptosisSalvia miltiorrhizaPharmacologyCell morphologyDepsidesSalvia miltiorrhizaCell Line TumorDrug DiscoveryCell AdhesionmedicineHumansLymphocytesCells CulturedMembrane Potential MitochondrialPharmacologybusiness.industryGene Expression ProfilingCell CycleNF-kappa BPrecursor Cell Lymphoblastic Leukemia-LymphomaCell cycleMolecular biologyDrug Resistance MultipleMolecular Docking Simulationmedicine.anatomical_structureCinnamatesDrug Resistance NeoplasmApoptosisComet AssayReactive Oxygen SpeciesbusinessDNA DamageJournal of Ethnopharmacology
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Cytotoxicity of 40 Egyptian plant extracts targeting mechanisms of drug-resistant cancer cells

2019

Abstract Background The multidrug resistance (MDR) phenotype encounters a major challenge to the success of established chemotherapy in cancer patients. We hypothesized that cytotoxic medicinal plants with novel phytochemicals can overcome MDR and kill MDR-cells with similar efficacy as drug sensitive cells. Purpose We evaluated plant extracts from an unexplored ecosystem in Egypt with unusual climate and nutrient conditions for their activity against sensitive and multidrug-resistant cancer cell lines. Material and methods/study design Methylene chloride: methanol (1:1) and methanol: H2O (7:3) extracts of 40 plants were prepared resulting in a sum of 76 fraction containing compounds with v…

Programmed cell deathCell SurvivalPhytochemicalsPharmaceutical ScienceApoptosisCentaureaWithaniaPulicariaMagnoliopsida03 medical and health sciences0302 clinical medicineCell Line TumorNeoplasmsDrug DiscoveryHumansCytotoxic T cellViability assayCytotoxicity030304 developmental biologyMembrane Potential MitochondrialPharmacology0303 health sciencesPlants MedicinalbiologyPlant ExtractsChemistryWithaniabiology.organism_classificationAntineoplastic Agents PhytogenicMolecular biologyDrug Resistance MultipleMultiple drug resistanceComplementary and alternative medicineDrug Resistance NeoplasmCell culture030220 oncology & carcinogenesisCancer cellMolecular MedicineEgyptReactive Oxygen SpeciesPhytotherapyPhytomedicine
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Therapeutic targeting of apoptotic pathways in cancer.

2006

Programmed cell death (apoptosis) is a key tumor suppressor mechanism. Consequently, most if not all cancers develop mechanisms to abolish or circumvent this genetic program. Besides enabling malignant transformation and tumor progression, defects in apoptosis can result in resistance to cytotoxic cancer therapies. Much progress has been made in the delineation of the molecular pathways leading to apoptosis. This allows the identification of target molecules and lead compounds to develop novel therapies, which make use of this intrinsic death program for the treatment of cancer. Here, we review the current understanding of apoptotic signal transduction pathways, and strategies of their ther…

Programmed cell deathClinical BiochemistryAntineoplastic AgentsApoptosislaw.inventionMalignant transformationDrug Delivery SystemslawNeoplasmsDrug DiscoverymedicineAnimalsHumansPharmacologyMechanism (biology)business.industryCancermedicine.diseaseApoptosisTumor progressionGene TargetingCancer researchMolecular MedicineSuppressorSignal transductionbusinessSignal TransductionCurrent drug targets
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