Search results for "plastic"

showing 10 items of 7296 documents

Synthesis of Combretastatin A-4 and 3′-Aminocombretastatin A-4 derivatives with Aminoacid Containing Pendants and Study of their Interaction with Tub…

2020

Natural product combretastatin A-4 (CA-4) and its nitrogenated analogue 3&prime

Vascular Endothelial Growth Factor ACell cycle checkpoint<i>htert</i>Pharmaceutical ScienceApoptosisAnalytical Chemistrychemistry.chemical_compound0302 clinical medicineDrug DiscoveryStilbenesc-<i>myc</i>Telomerase0303 health sciences<i>vegf</i>biologyNeovascularization PathologicChemistry3′-aminocombretastatin a-4Cell cycle<i>c-Myc</i>VEGFc-MycBiochemistryChemistry (miscellaneous)030220 oncology & carcinogenesisMCF-7 CellsMolecular Medicinecytotoxicitycell cyclehTERTHT29 CellsArticleProto-Oncogene Proteins c-mycmicrotubuleslcsh:QD241-44103 medical and health sciencesStructure-Activity Relationshiplcsh:Organic chemistryMicrotubuleCell Line TumorHumansPhysical and Theoretical Chemistry030304 developmental biologyCell ProliferationCombretastatinCombretastatin A-4Cell growthOrganic ChemistryAntineoplastic Agents PhytogenicTubulintubulinCell cultureA549 Cellsbiology.proteinM Phase Cell Cycle Checkpointscombretastatin a-4Drug Screening Assays AntitumorMolecules
researchProduct

Arthrinins A–D: Novel diterpenoids and further constituents from the sponge derived fungus Arthrinium sp.

2011

Bioassay-guided fractionation of a methanolic extract of the fungus Arthrinium sp., isolated from the Mediterranean sponge Geodia cydonium, afforded 10 natural products including five new diterpenoids, arthrinins A-D (1-4) and myrocin D (5). In addition, five known compounds were obtained, which included myrocin A (6), norlichexanthone (7), anomalin A (8), decarboxycitrinone (9) and 2,5-dimethyl-7-hydroxychromone (10). The structures of all isolated compounds were unambiguously elucidated based on extensive 1D and 2D NMR and HR-MS analyzes. The absolute configuration of arthrinins A-D (1-4) was established by the convenient Mosher method performed in NMR tubes and by interpretation of the R…

Vascular Endothelial Growth Factor AClinical BiochemistryPharmaceutical ScienceAntineoplastic AgentsBiochemistryMiceAscomycotaCell Line TumorNeoplasmsDrug DiscoveryAnimalsHumansMTT assayCytotoxicityProtein Kinase InhibitorsMolecular BiologyNeovascularization PathologicKinaseChemistryOrganic ChemistryTerpenoidIn vitroPoriferaEndothelial stem cellVascular endothelial growth factor ABiochemistryCell cultureMolecular MedicineDiterpenesProtein KinasesBioorganic &amp; Medicinal Chemistry
researchProduct

The impact of tumor nitric oxide production on VEGFA expression and tumor growth in a zebrafish rat glioma xenograft model.

2015

International audience; To investigate the effect of nitric oxide on tumor development, we established a rat tumor xenograft model in zebrafish embryos. The injected tumor cells formed masses in which nitric oxide production could be detected by the use of the cell-permeant DAF-FM-DA (diaminofluorophore 4-amino-5-methylamino-2'-7'-difluorofluorescein diacetate) and DAR-4M-AM (diaminorhodamine-4M). This method revealed that nitric oxide production could be co-localized with the tumor xenograft in 46% of the embryos. In 85% of these embryos, tumors were vascularized and blood vessels were observed on day 4 post injection. Furthermore, we demonstrated by qRT-PCR that the transplanted glioma ce…

Vascular Endothelial Growth Factor AMESH: Cyclin D1lcsh:MedicineMESH : Analysis of VarianceMESH: Flow Cytometry[ SDV.IMM.IA ] Life Sciences [q-bio]/Immunology/Adaptive immunologyBenzoates[SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity[ SDV.CAN ] Life Sciences [q-bio]/CancerMESH: GliomaMESH: Reverse Transcriptase Polymerase Chain ReactionCyclin D1MESH: Animalslcsh:ScienceZebrafishMESH : RatsReverse Transcriptase Polymerase Chain ReactionMESH: Real-Time Polymerase Chain ReactionHistological TechniquesMESH : Reverse Transcriptase Polymerase Chain ReactionImidazolesGliomaMESH: Gene Expression Regulation NeoplasticFlow CytometryMESH : Cyclin D1Gene Expression Regulation NeoplasticMESH : Nitric Oxide[SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunologyMESH : Vascular Endothelial Growth Factor AHeterograftsMESH : Histological TechniquesMESH: ImidazolesResearch ArticleMESH : BenzoatesMESH: RatsMESH : Flow CytometryMESH : Gene Expression Regulation NeoplasticMESH : Real-Time Polymerase Chain ReactionMESH : Zebrafish[SDV.CAN]Life Sciences [q-bio]/CancerMESH: Histological TechniquesMESH : HeterograftsNitric OxideReal-Time Polymerase Chain ReactionMESH : ImidazolesMESH: Analysis of VarianceAnimalsMESH: Zebrafish[ SDV.IMM.II ] Life Sciences [q-bio]/Immunology/Innate immunityAnalysis of VarianceMESH: Vascular Endothelial Growth Factor Alcsh:RMESH: BenzoatesRatsMESH : GliomaMESH: Nitric Oxidelcsh:QMESH: HeterograftsMESH : Animals
researchProduct

Anticancer therapy-induced vascular toxicity: VEGF inhibition and beyond

2017

Cardiotoxicity induced by chemotherapeutic agents and radiotherapy is a growing problem. In recent years, an increasing number of new drugs with targeted action have been designed. These molecules, such as monoclonal antibodies and tyrosine kinase inhibitors, can cause different type of toxicities compared to traditional chemotherapy. However, they can also cause cardiac complications such as heart failure, arterial hypertension, QT interval prolongation and arrhythmias. Currently, a field of intense research is the vascular toxicity induced by new biologic drugs, particularly those which inhibit vascular endothelial growth factor (VEGF) and its receptor (VEGF-R) and other tyrosine kinases.…

Vascular Endothelial Growth Factor APathologymedicine.medical_specialtyHeart Diseasesmedicine.medical_treatmentVascular toxicity VEGF cardiotoxicity new target therapy chemotherapy radiotherapy cardio-oncologyAntineoplastic Agents030204 cardiovascular system & hematologyQT intervalCardiooncology03 medical and health scienceschemistry.chemical_compoundCardio-oncology; Cardiotoxicity; Chemotherapy; New target therapy; Radiotherapy; Vascular toxicity; VEGF; Medicine (all); Cardiology and Cardiovascular Medicine0302 clinical medicineVascularReceptorsmedicineAnimalsHumansChemotherapyEndotheliumNew target therapyChemotherapyCardiotoxicityRadiotherapybusiness.industryVascular Endothelial Growth FactorMedicine (all)Cardiooncology; Vascular toxicity; New target therapyCardio-oncology; Cardiotoxicity; Chemotherapy; New target therapy; Radiotherapy; Vascular toxicity; VEGF; Animals; Antineoplastic Agents; Cardiotoxicity; Endothelium Vascular; Heart Diseases; Humans; Reactive Oxygen Species; Receptors Vascular Endothelial Growth Factor; Vascular Endothelial Growth Factor Amedicine.diseaseVEGFCardiotoxicityVascular endothelial growth factorRadiation therapyCardio-oncologyVascular endothelial growth factor AReceptors Vascular Endothelial Growth Factorchemistry030220 oncology & carcinogenesisHeart failureCancer researchEndothelium VascularVascular toxicityReactive Oxygen SpeciesCardiology and Cardiovascular MedicinebusinessTyrosine kinaseInternational Journal of Cardiology
researchProduct

Hypoxia-stimulated expression of angiogenic growth factors in cervical cancer cells and cervical cancer-derived fibroblasts

2001

It is generally accepted that local growth of solid tumors and their ability to establish distant metastases are dependent on the formation of new blood vessels arising from preexisting ones (angiogenesis). The angiogenic response of the host is mediated by angiogenic molecules that are released from cancer and normal stroma cells, especially fibroblasts. The goal of the present study was to quantitatively compare the expression of the two most important angiogenic growth factors (VEGF, angiogenin) of cervical cancer cells (HeLa and Me-180) with that of cervical cancer-derived fibroblasts (from one tumor/patient) under defined normoxic and hypoxic conditions in vitro. The growth kinetics of…

Vascular Endothelial Growth Factor APathologymedicine.medical_specialtyStromal cellAngiogeninAngiogenesismedicine.medical_treatmentCellUterine Cervical NeoplasmsEnzyme-Linked Immunosorbent AssayEndothelial Growth FactorsHeLamedicineHumansHypoxiaLymphokinesNeovascularization PathologicbiologyVascular Endothelial Growth FactorsGrowth factorObstetrics and GynecologyRibonuclease PancreaticFibroblastsbiology.organism_classificationIn vitroGene Expression Regulation NeoplasticKineticsmedicine.anatomical_structureOncologyCell cultureCancer researchFemaleCell DivisionHeLa CellsInternational Journal of Gynecological Cancer
researchProduct

High levels of HIF-2α highlight an immature neural crest-like neuroblastoma cell cohort located in a perivascular niche

2007

High HIF-2alpha protein levels in the sympathetic nervous system-derived childhood tumour neuroblastoma as well as immature phenotype correlate to unfavourable outcome. Here we show that a small subset of perivascularly located, strongly HIF-2alpha-positive tumour cells (MYCN amplified) lacks expression of differentiation markers, but expresses neural crest and early sympathetic progenitor marker genes such as Notch-1, HES-1, c-Kit, dHAND, and vimentin. HIF-2alpha- and CD68-positive tumour-associated macrophages were frequently found close to the immature and HIF-2alpha-positive neuroblastoma cells and as VEGF levels are high in the perivascular niche, we hypothesize that neuroblastoma neur…

Vascular Endothelial Growth Factor APathologymedicine.medical_specialtySympathetic Nervous SystemAngiogenesisVimentinPathology and Forensic MedicineNeuroblastomaNeuroblastomaBasic Helix-Loop-Helix Transcription FactorsTumor Cells CulturedmedicineHumansMacrophageProgenitorOncogene ProteinsN-Myc Proto-Oncogene ProteinNeovascularization PathologicbiologyMacrophagesNuclear ProteinsNeural crestmedicine.diseasePhenotypeCell HypoxiaNeoplasm ProteinsNeural CrestNeoplastic Stem Cellsbiology.proteinCancer researchStem cellThe Journal of Pathology
researchProduct

Predicting efficacy and toxicity in the era of targeted therapy: focus on anti-EGFR and anti-VEGF molecules

2011

The treatment of solid malignancies includes various target drugs, such as monoclonal antibodies and tyrosine kinase inhibitors, which exert their effect alone or in combination with chemotherapy. The main part of these molecules have a target on proteins of EGFR and VEGF pathways. The particular toxicity profile and the financial impact, deriving from the application of these agents in cancer treatment, prompted a lot of researches to define predictive factors of their efficacy. Various biomarker were identified among the components of the targeted pathways. However just few studies allowed to identify specific factors to predict the toxicity of these drugs. In this review EGFR and VEGF-re…

Vascular Endothelial Growth Factor Amedicine.drug_classSettore MED/06 - Oncologia Medicamedicine.medical_treatmentClinical BiochemistryAngiogenesis InhibitorsAntineoplastic AgentsPharmacologyMonoclonal antibodyTargeted therapyAntineoplastic AgentNeoplasmsProtein-Tyrosine KinasemedicineHumansAngiogenesis Inhibitors; Antibodies Monoclonal; Antineoplastic Agents; Humans; Neoplasms; Protein-Tyrosine Kinases; Receptor Epidermal Growth Factor; Treatment Outcome; Vascular Endothelial Growth Factor ATarget therapyPharmacologyAnti vegfChemotherapybusiness.industryAntibodies MonoclonalProtein-Tyrosine KinasesErbB ReceptorsTreatment OutcomeToxicityCancer researchBiomarker (medicine)NeoplasmReceptor Epidermal Growth FactorbusinessTyrosine kinaseAngiogenesis InhibitorHuman
researchProduct

Tyrosine Phosphorylation Modulates the Vascular Responses of Mesenteric Arteries from Human Colorectal Tumors

2013

The aim of this study was to analyze whether tyrosine phosphorylation in tumoral arteries may modulate their vascular response. To do this, mesenteric arteries supplying blood flow to colorectal tumors or to normal intestine were obtained during surgery and prepared for isometric tension recording in an organ bath. Increasing tyrosine phosphorylation with the phosphatase inhibitor, sodium orthovanadate produced arterial contraction which was lower in tumoral than in control arteries, whereas it reduced the contraction to noradrenaline in tumoral but not in control arteries and reduced the relaxation to bradykinin in control but not in tumoral arteries. Protein expression of VEGF-A and of th…

Vascular Endothelial Growth Factor Amedicine.medical_specialtyContraction (grammar)Article SubjectMedicinaBradykininlcsh:MedicineBiologyGeneral Biochemistry Genetics and Molecular BiologyTyrosine phosphorylationchemistry.chemical_compoundOrgan Culture TechniquesInternal medicinemedicineHumansPhosphorylationTyrosineSodium orthovanadateMesenteric arteriesVascular Endothelial Growth Factor Receptor-1Neovascularization PathologicGeneral Immunology and Microbiologylcsh:RTyrosine phosphorylationGeneral MedicineMesenteric ArteriesGene Expression Regulation NeoplasticVascular endothelial growth factor AEndocrinologymedicine.anatomical_structurechemistryTyrosinePhosphorylationVanadatesColorectal NeoplasmsResearch ArticleBioMed Research International
researchProduct

Regulation of NOS expression in vascular diseases

2020

Nitric oxide synthases (NOS) are the major sources of nitric oxide (NO), a small bioactive molecule involved in the regulation of many cellular processes. One of the most prominent functions of NO is regulation of vasodilatation and thereby control of blood pressure. Most important for vascular tone is NOS3. Endothelial NOS3-generated NO diffuses into the vascular smooth muscle cells, activates the soluble guanylate cyclase resulting in enhanced cGMP concentrations and smooth muscle cell relaxation. However, more and more evidence exist that also NOS1 and NOS2 contribute to vascular function. We summarize the current knowledge about the regulation of NOS expression in the vasculature by tra…

Vascular smooth muscleNitric Oxide Synthase Type IIINOS1CellNitric Oxide Synthase Type IIBlood PressureVasodilationInflammationNitric Oxide Synthase Type INitric OxideMuscle Smooth VascularNitric oxidechemistry.chemical_compoundmedicineAnimalsHumansProtein IsoformsVascular DiseasesRNA Processing Post-TranscriptionalInflammationRegulation of gene expressionInnate immune systemAtherosclerosisImmunity InnateCell biologyGene Expression Regulation Neoplasticmedicine.anatomical_structurechemistryNitric Oxide Synthasemedicine.symptomProtein Processing Post-TranslationalFrontiers in Bioscience-Landmark
researchProduct

Identification and optimization of small molecule antagonists of vasoactive intestinal peptide receptor-1 (VIPR1).

2012

Identification, synthesis and structure-activity relationship of small-molecule VIPR1 antagonists encompassing two chemical series are described.

Vasoactive intestinal peptide (VIP)Settore MED/09 - Medicina InternaReceptors Vasoactive Intestinal Polypeptide Type IClinical BiochemistryVasoactive intestinal peptidePharmaceutical ScienceAntineoplastic AgentsThiophenesBiochemistrySmall Molecule LibrariesStructure-Activity RelationshipCell Line TumorDrug DiscoveryStructure–activity relationshipHumansReceptorMolecular BiologyChemistryVasoactive intestinal peptide receptorOrganic ChemistryBiphenyl CompoundsSmall Molecule LibrariesSmall moleculeHigh-Throughput Screening AssaysBiochemistryCell cultureVasoactive intestinal peptide receptor (VIPR)Molecular MedicineDrug Screening Assays AntitumorVIPR1Bioorganicmedicinal chemistry letters
researchProduct