Search results for " Drug"

showing 10 items of 3138 documents

Cancer therapy and treatments during COVID-19 era

2020

The COVID-19 pandemic has put a serious strain on health treatments as well at the economies of many nations. Unfortunately, there is not currently available vaccine for SARS-Cov-2/COVID-19. Various types of patients have delayed treatment or even routine check-ups and we are adapting to a virtual world. In many cases, surgeries are delayed unless they are essential. This is also true with regards to cancer treatments and screening. Interestingly, some existing drugs and nutraceuticals have been screened for their effects on COVID-19. Certain FDA approved drugs, vitamin, natural products and trace minerals may be repurposed to treat or improve the prevention of COVID-19 infections and disea…

0301 basic medicineCancer ResearchDiseaseComorbidityAntineoplastic Agent0302 clinical medicineRepurposing approved drugNeoplasmsPandemicMedicineViralCancerNatural productsVitaminsSpike GlycoproteinHost-Pathogen InteractionDrug repositioning030220 oncology & carcinogenesisHost-Pathogen InteractionsSpike Glycoprotein CoronavirusMolecular MedicineNutraceuticalAngiotensin-Converting Enzyme 2NutraceuticalsCoronavirus InfectionsHumanHydroxychloroquineSignal Transductionmedicine.medical_specialtyCoronavirus disease 2019 (COVID-19)Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)Pneumonia ViralAntineoplastic AgentsPeptidyl-Dipeptidase AAntiviral AgentsNatural productVitaminArticle03 medical and health sciencesBetacoronavirusGeneticsHumansIntensive care medicineMolecular BiologyPandemicsTrace ElementAntiviral AgentBetacoronaviruCoronavirus Infectionbusiness.industrySARS-CoV-2CanceRepurposing approved drugsDrug RepositioningrNatural productsCancerCOVID-19Pneumoniamedicine.diseaseComorbidityReview articleTrace ElementsCoronavirus030104 developmental biologyGene Expression RegulationSettore BIO/14 - FarmacologiaNeoplasmbusinessSpike Glycoprotein Coronaviru
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Doxorubicin anti-tumor mechanisms include Hsp60 post-translational modifications leading to the Hsp60/p53 complex dissociation and instauration of re…

2017

Hsp60 is a pro-carcinogenic chaperonin in certain tumor types by interfering with apoptosis and with tumor cell death. In these tumors, it is not known whether or not doxorubicin anti-tumor effects include a blockage of the pro-carcinogenic action of this protein. We used the human lung mucoepidermoid cell line NCI-H292 and different doses of doxorubicin to measure cell viability, cell cycle progression, cell senescence indicators, Hsp60 levels and its post-translational modifications as well as the release of the chaperonin into the extracellular environment. Cell viability was reduced in relation to doxorubicin dose and this was paralleled by the appearance of cell senescence markers. Con…

0301 basic medicineCancer ResearchLung NeoplasmsChaperoninsCellApoptosismedicine.disease_causeHistones0302 clinical medicineCellular SenescenceAntibiotics AntineoplasticAcetylationG2 Phase Cell Cycle Checkpointsmedicine.anatomical_structureOncology030220 oncology & carcinogenesisCell agingIntracellularProtein BindingSignal TransductionSenescenceCyclin-Dependent Kinase Inhibitor p21animal structuresCell Survivalchemical and pharmacologic phenomenaBiologycomplex mixturesMitochondrial ProteinsDoxorubicin Hsp60 Acetylation Ubiquitination p53 Replicative senescence03 medical and health sciencesDoxorubicin; Hsp60; p53; replicative senescence; post-translational modificationsCell Line TumormedicineHumansCell Proliferationdoxorubicin p53 Hsp60Dose-Response Relationship DrugCell growthfungiUbiquitinationChaperonin 60Molecular biology030104 developmental biologyAcetylationApoptosisDoxorubicinProteolysisCancer researchCarcinoma MucoepidermoidTumor Suppressor Protein p53CarcinogenesisProtein Processing Post-Translational
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Breast Cancer Organoids Model Patient-Specific Response to Drug Treatment

2020

Tumor organoids are tridimensional cell culture systems that are generated in vitro from surgically resected patients&rsquo

0301 basic medicineCancer ResearchMechanotransductionBreast cancer; Dasatinib; Drug testing; Heterogeneity; Mechanotransduction; Patient‐derived tumor organoids; Statin; YAPPatient‐derived tumor organoidCellDasatinibDrug resistanceSettore MED/08 - Anatomia PatologicaBiologylcsh:RC254-282Article03 medical and health sciencesBreast cancer0302 clinical medicineBreast cancerbreast cancermedicineOrganoidSettore MED/05 - Patologia Clinicadasatinibdrug testingmechanotransductionpatient-derived tumor organoidsGenetic heterogeneitystatinStatinDrug testingBreast cancerDasatinib Drug testing Drug testing Heterogeneity Patient‐derived tumor organoids Statin YAPmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensIn vitroDasatinib030104 developmental biologymedicine.anatomical_structureOncologyCell culture030220 oncology & carcinogenesisCancer researchPatient‐derived tumor organoidsYAPHeterogeneityheterogeneitymedicine.drugCancers
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Stem-cell derived hepatocyte-like cells for the assessment of drug-induced liver injury.

2019

Drug-induced liver injury is a major cause of drug discovery failure in clinical trials and a leading cause of liver disease. Current preclinical drug testing does not predict hepatotoxicity which highlights the importance of developing highly predictive cell-based models. The use of stem cell technology and differentiation into hepatocyte-like cells (HLCs) could provide a stable source of hepatocytes for multiple applications, including drug screening. HLCs derived from both embryonic and induced pluripotent stem cells have been used to accurately predict hepatotoxicity as well as to test individual-specific toxicity. Although there are still many limitations, mainly related to the lack of…

0301 basic medicineCancer ResearchPopulationCellInduced Pluripotent Stem CellsDrug Evaluation PreclinicalBiology03 medical and health sciencesLiver disease0302 clinical medicinemedicineAnimalsHumansInduced pluripotent stem celleducationMolecular BiologyEmbryonic Stem Cellseducation.field_of_studyDrug discoveryCell DifferentiationCell Biologymedicine.diseaseEmbryonic stem cell030104 developmental biologymedicine.anatomical_structurePhenotypeHepatocyteCancer researchHepatocytesStem cellChemical and Drug Induced Liver Injury030217 neurology & neurosurgeryDevelopmental BiologyDifferentiation; research in biological diversity
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Abilities of β-Estradiol to interact with chemotherapeutic drugs, signal transduction inhibitors and nutraceuticals and alter the proliferation of pa…

2019

Improving the effects of chemotherapy and reducing the side effects are important goals in cancer research. Various approaches have been examined to enhance the effectiveness of chemotherapy. For example, signal transduction inhibitors or hormonal based approaches have been included with chemo- or radio-therapy. MIA-PaCa-2 and BxPC-3 pancreatic ductal adenocarcinoma (PDAC) cells both express the estrogen receptor (ER). The effects of β-estradiol on the growth of PDAC cells has not been examined yet the ER is expressed in PDAC cells. We have examined the effects of combining β-estradiol with chemotherapeutic drugs, signal transcription inhibitors, natural products and nutraceuticals on PDAC.…

0301 basic medicineCancer Researchendocrine system diseasesβ estradiolmedicine.medical_treatmentβ-EstradiolEstrogen receptorAntineoplastic AgentsNatural product03 medical and health sciencesFood-Drug Interactions0302 clinical medicineNutraceuticalPancreatic cancerCell Line TumorGeneticsmedicineHumansMolecular BiologyChemotherapeutic drugCell ProliferationChemotherapyNatural products?-EstradiolEstradiolbusiness.industryQUIMIOTERÁPICOSChemotherapeutic drugs; Natural products; Nutraceuticals; Pancreatic cancer; β-EstradiolPancreatic cancerMiddle Agedmedicine.diseasedigestive system diseasesPancreatic Neoplasms030104 developmental biology030220 oncology & carcinogenesisDietary SupplementsCancer researchSettore BIO/14 - FarmacologiaMolecular MedicineChemotherapeutic drugsFemaleChemotherapeutic drugsNutraceuticalsNutraceuticalSignal transductionbusinessHormoneCarcinoma Pancreatic DuctalSignal TransductionAdvances in biological regulation
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Tumor Microenvironment And Epithelial Mesenchymal Transition As Targets To Overcome Tumor Multidrug Resistance

2020

It is well established that multifactorial drug resistance hinders successful cancer treatment. Tumor cell interactions with the tumor microenvironment (TME) are crucial in epithelial-mesenchymal transition (EMT) and multidrug resistance (MDR). TME-induced factors secreted by cancer cells and cancer-associated fibroblasts (CAFs) create an inflammatory microenvironment by recruiting immune cells. CD11b+/Gr-1+ myeloid-derived suppressor cells (MDSCs) and inflammatory tumor associated macrophages (TAMs) are main immune cell types which further enhance chronic inflammation. Chronic inflammation nurtures tumor-initiating/cancer stem-like cells (CSCs), induces both EMT and MDR leading to tumor re…

0301 basic medicineCancer Researchmedicine.medical_treatmentMultidrug resistanceTargeted therapyTargeted therapy0302 clinical medicineCancer-Associated FibroblastsNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsTumor-Associated MacrophagesTumor MicroenvironmentPharmacology (medical)HypoxiaTOR Serine-Threonine KinasesSmall moleculesChemotherapy ; Hypoxia ; Inflammation ; Microenvironment ; Multidrug resistance ; Small molecules ; Targeted therapy.Drug Resistance Multiple3. Good healthDNA DemethylationGene Expression Regulation NeoplasticInfectious DiseasesOncology030220 oncology & carcinogenesisInflammation MediatorsEpithelial-Mesenchymal TransitionStromal cellMicroenvironmentBiologyProinflammatory cytokine03 medical and health sciencesCell Line TumormedicineAnimalsHumansChemotherapyEpithelial–mesenchymal transitionPharmacologyInflammationTumor microenvironmentCancerHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseHistone Deacetylase InhibitorsMultiple drug resistanceDisease Models Animal030104 developmental biologyDrug Resistance NeoplasmCancer cellCancer research
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Personalized Medicine: Recent Progress in Cancer Therapy

2020

Translational research has revolutionized how we develop new treatments for cancer patients. The change from an organ-centric concept guiding treatment choice towards deep molecular analysis, driving a personalized approach, is one of the most important advances of modern oncology. Several tools such as next generation sequencing and RNA sequencing have greatly improved the capacity to detect predictive and prognostic molecular alterations. Detection of gene mutations, amplifications, and fusions has therefore altered the history of several diseases in both a localized and metastatic setting. This shift in perspective, in which attention is focused on the specific molecular alterations of t…

0301 basic medicineCancer Researchprecision medicineCancer therapyTranslational researchComputational biologyReviewGene mutationTumor heterogeneitylcsh:RC254-28203 medical and health sciences0302 clinical medicineMedicinetranslational oncologybusiness.industryCancerpersonalized medicinePrecision medicinemedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologyOncology030220 oncology & carcinogenesisIdentification (biology)new drug developmentPersonalized medicinebusinessCancers
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Cytotoxic effects induced by patulin, deoxynivalenol and toxin T2 individually and in combination in hepatic cells (HepG2).

2018

Abstract Patulin (PAT), deoxynivalenol (DON) and toxin T-2 (T-2) are mycotoxins distributed worldwide in food and feed. Cytotoxicity of the three mycotoxins individually or in combination in human hepatocellular carcinoma (HepG2) cells was evaluated by MTT assay over 24, 48 and 72 h of exposure. The concentration ranges used were 0.625–15 μM for DON, 1.25–50 nM for T-2 and 0.45–7.5 μM for PAT. The IC 50 values obtained ranged from 9.30 to 2.53 μM, from 33.69 to 44.37 nM and from 2.66 to 1.17 μM for DON, T-2 and PAT, respectively. The most cytotoxic mycotoxin to HepG2 cells was T-2 followed by PAT and DON. The combination ratios used for the mixtures were 1:3 (DON: T-2), 1:5 (DON: PAT), 1:1.…

0301 basic medicineCell SurvivalComplex MixturesToxicologymedicine.disease_causePatulin03 medical and health scienceschemistry.chemical_compoundInhibitory Concentration 500404 agricultural biotechnologymedicineCytotoxic T cellHumansMTT assayDrug InteractionsCytotoxicityMycotoxinDose-Response Relationship DrugToxin04 agricultural and veterinary sciencesGeneral MedicineHep G2 CellsMycotoxinsmedicine.disease040401 food scienceMolecular biologyDrug CombinationsT-2 Toxin030104 developmental biologyPatulinchemistryLiverHepatocellular carcinomaHepatic stellate cellTrichothecenesFood ScienceFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association
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Imatinib-Loaded Micelles of Hyaluronic Acid Derivatives for Potential Treatment of Neovascular Ocular Diseases

2018

In this work, new micellar systems able to cross corneal barrier and to improve the permeation of imatinib free base were prepared and characterized. HA-EDA-C-16, HA-EDA-C-16-PEG, and HA-EDA-C-16-CRN micelles were synthesized starting from hyaluronic acid (HA), ethylenediamine (EDA), hexadecyl chains (C-16), polyethylene glycol (PEG), or L-carnitine (CRN). These nanocarriers showed optimal particle size and mucoadhesive properties. Imatinib-loaded micelles were able to interact with corneal barrier and to promote imatinib transcorneal permeation and penetration. In addition, a study was conducted to understand the in vitro imatinib inhibitory effect on a choroidal neovascularization process…

0301 basic medicineCell SurvivalDrug CompoundingPharmaceutical ScienceAdministration Ophthalmic02 engineering and technologyPolyethylene glycolMicellePermeabilityCell LinePolyethylene GlycolsCornea03 medical and health scienceschemistry.chemical_compoundocular drug delivery hyaluronic acid polymeric micelles imatinib transcorneal permeation ocular neovascular diseasesCarnitinehemic and lymphatic diseasesDrug DiscoveryHyaluronic acidPEG ratiomedicineocular drug delivery; hyaluronic acid; polymeric micelles; imatinib; transcorneal permeation; ocular neovascular diseasesAnimalsHumansHyaluronic AcidParticle SizeProtein Kinase InhibitorsneoplasmsMicellesDrug CarriersEndothelial CellsImatinibPermeation021001 nanoscience & nanotechnologyEthylenediaminesIn vitroChoroidal NeovascularizationDrug Liberation030104 developmental biologychemistrySettore CHIM/09 - Farmaceutico Tecnologico ApplicativoBiophysicsImatinib MesylateMolecular Medicinelipids (amino acids peptides and proteins)CattleNanocarriers0210 nano-technologymedicine.drug
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Extracellular histones activate autophagy and apoptosis via mTOR signaling in human endothelial cells.

2018

Circulating histones have been proposed as targets for therapy in sepsis and hyperinflammatory symptoms. However, the proposed strategies have failed in clinical trials. Although different mechanisms for histone-related cytotoxicity are being explored, those mediated by circulating histones are not fully understood. Extracellular histones induce endothelial cell death, thereby contributing to the pathogenesis of complex diseases such as sepsis and septic shock. Therefore, the comprehension of cellular responses triggered by histones is capital to design effective therapeutic strategies. Here we report how extracellular histones induce autophagy and apoptosis in a dose-dependent manner in cu…

0301 basic medicineCell SurvivalEndothelial cellsFisiologiaApoptosisAMP-Activated Protein KinasesHistones03 medical and health sciencesExtracellularAutophagyHuman Umbilical Vein Endothelial CellsAutophagy-Related Protein-1 HomologHumansMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwaybiologyDose-Response Relationship DrugChemistryTOR Serine-Threonine KinasesAutophagyIntracellular Signaling Peptides and ProteinsAMPKNuclear ProteinsCirculating histonesCell biologyToll-like receptorsEndothelial stem cell030104 developmental biologyHistoneApoptosisbiology.proteinMolecular MedicineProto-Oncogene Proteins c-aktSignal TransductionBiochimica et biophysica acta. Molecular basis of disease
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