Search results for "antineoplastic"

showing 10 items of 2217 documents

Endothelin-1-Mediated Drug Resistance in EGFR-Mutant Non-Small Cell Lung Carcinoma.

2020

Abstract Progression on therapy in non-small cell lung carcinoma (NSCLC) is often evaluated radiographically, however, image-based evaluation of said therapies may not distinguish disease progression due to intrinsic tumor drug resistance or inefficient tumor penetration of the drugs. Here we report that the inhibition of mutated EGFR promotes the secretion of a potent vasoconstrictor, endothelin-1 (EDN1), which continues to increase as the cells become resistant with a mesenchymal phenotype. As EDN1 and its receptor (EDNR) is linked to cancer progression, EDNR-antagonists have been evaluated in several clinical trials with disappointing results. These trials were based on a hypothesis that…

Vascular Endothelial Growth Factor ACancer ResearchLung NeoplasmsAmbrisentanOncology and CarcinogenesisDrug ResistanceBiological AvailabilityAntineoplastic AgentsDrug resistanceCell LineMiceErlotinib HydrochlorideGefitinibIn vivomedicineAnimalsHumansOncology & CarcinogenesisNon-Small-Cell LungProtein Kinase InhibitorsLungCancerTumor microenvironmentTumorEndothelin-1business.industryCarcinomaLung CancerCancerEvaluation of treatments and therapeutic interventionsGefitinibmedicine.diseaseEndothelin 1Xenograft Model Antitumor AssaysErbB ReceptorsOncologyVasoconstriction5.1 Pharmaceuticals6.1 PharmaceuticalsCancer cellMutationCancer researchNeoplasmDevelopment of treatments and therapeutic interventionsbusinessmedicine.drug
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An Open-Label Phase II Study Evaluating the Safety and Efficacy of Ramucirumab Combined With mFOLFOX-6 as First-Line Therapy for Metastatic Colorecta…

2014

Abstract Author Summary Background. Vascular endothelial growth factor (VEGF) and VEGF receptor 2 (VEGFR-2) are believed to mediate angiogenesis in colorectal cancer (CRC). Ramucirumab (RAM; IMC-1121B) is a human IgG1 monoclonal antibody that inhibits VEGF ligand binding to VEGFR-2, inhibiting VEGFR-2 activation and signaling. Methods. Patients with metastatic CRC, Eastern Cooperative Oncology Group performance status 0–1, and adequate organ function who had not received chemotherapy for metastatic disease received RAM and the modified FOLFOX-6 regimen every 2 weeks. Endpoints included progression-free survival (PFS), objective response rate, overall survival, and safety. The sample size wa…

Vascular Endothelial Growth Factor ACancer ResearchPathologymedicine.medical_specialtyOrganoplatinum CompoundsAngiogenesisColorectal cancerLeucovorinAntibodies Monoclonal HumanizedDisease-Free SurvivalDrug Administration ScheduleRamucirumabchemistry.chemical_compoundAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansNeoplasm Metastasisbusiness.industryClinical Trial ResultsAntibodies MonoclonalKinase insert domain receptormedicine.diseaseVascular Endothelial Growth Factor Receptor-2Vascular endothelial growth factorVascular endothelial growth factor ATreatment OutcomeOncologychemistryFluorouracilMonoclonalCancer researchFluorouracilbusinessColorectal Neoplasmsmedicine.drugProtein Binding
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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
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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
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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
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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
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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
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alpha-Tocopherol, MDA-HNE and 8-OHdG levels in liver and heart mitochondria of adriamycin-treated rats fed with alcohol-free beer.

2008

Different studies indicate that oxidative stress and mitochondrial damage are key factors in different pathogenic process. The aim of this study was to investigate the possible protective role of alcohol-free beer on adriamycin-induced (ADR) heart and liver toxicity using biomarkers of oxidative stress. This effect was compared with the effect of alcohol beer intake and with a control group. Rats were randomly divided into six groups. The first group received no adriamycin, was fed with water and was regarded as the control group; the second group was injected with a ADR (two cycles of 5mg/kg); the third and fourth groups were fed with alcohol-free and beer for 21 days, respectively and the…

VitaminMalemedicine.medical_specialtyAntioxidantmedicine.medical_treatmentalpha-TocopherolAlcoholMitochondria LiverToxicologymedicine.disease_causeMitochondria Heartchemistry.chemical_compoundInternal medicineMalondialdehydemedicineAnimalsTocopherolRats WistarHeart metabolismAldehydesEthanolAntibiotics AntineoplasticEthanolfood and beveragesBeerCentral Nervous System DepressantsDeoxyguanosineProteinsMalondialdehydeLipid MetabolismRatsOxidative StressEndocrinologychemistryBiochemistry8-Hydroxy-2'-DeoxyguanosineDoxorubicinIndicators and ReagentsOxidative stressDNA DamageToxicology
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Cytotoxic glycosides from the roots of Weigela x “Bristol Ruby”

2019

International audience; Seven oleanane-type glycosides were extracted and isolated by various chromatographic methods from the roots of Weigela x "Bristol Ruby" (1-7), six previously undescribed (1-6) and a known one (7). Their structures were assigned by spectroscopic analysis mainly 2D NMR and mass spectrometry (ESIMS). Selected triterpenoid glycosides (1-3, 6, 7) displayed a good cytotoxic activity against a mouse colon cancer cell line CT26.

WeigelaCytotoxicityPhytochemicalsOleanolic acid glycosidesMass spectrometryPlant Roots01 natural sciencesCaprifoliaceaeMiceTriterpenoidCell Line TumorDrug Discovery[SDV.IDA]Life Sciences [q-bio]/Food engineeringAnimalsCytotoxic T cellGlycosidesOleanolic AcidCytotoxicityCaprifoliaceaePharmacologychemistry.chemical_classificationChromatographyMolecular Structurebiology010405 organic chemistryGlycosideGeneral MedicineWeigela x “Bristol Ruby”biology.organism_classificationAntineoplastic Agents PhytogenicTriterpenesNMR3. Good health0104 chemical sciences010404 medicinal & biomolecular chemistrychemistryTwo-dimensional nuclear magnetic resonance spectroscopy
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Wee1 inhibition potentiates Wip1-dependent p53-negative tumor cell death during chemotherapy

2016

AbstractInactivation of p53 found in more than half of human cancers is often associated with increased tumor resistance to anti-cancer therapy. We have previously shown that overexpression of the phosphatase Wip1 in p53-negative tumors sensitizes them to chemotherapeutic agents, while protecting normal tissues from the side effects of anti-cancer treatment. In this study, we decided to search for kinases that prevent Wip1-mediated sensitization of cancer cells, thereby interfering with efficacy of genotoxic anti-cancer drugs. To this end, we performed a flow cytometry-based screening in order to identify kinases that regulated the levels of γH2AX, which were used as readout. Another criter…

Wip1ApoptosisCell Cycle ProteinsPharmacologyMESH: G2 Phase Cell Cycle CheckpointsHistonesMESH : PhosphorylationMiceMESH : Cell Cycle ProteinsMESH: AnimalsMESH: Tumor Suppressor Protein p53MESH: HistonesKinaseTp53 mutationsMESH : Mice Transgenic3. Good healthProtein Phosphatase 2CSurvival RateMESH : Antineoplastic AgentsH2ax phosphorylationP53 activationMESH: Protein Phosphatase 2CRNA InterferenceMESH : Colorectal NeoplasmsMESH : Carrier ProteinsHistone H2axMESH: MitochondriaImmunologyHuman fibroblastsMESH: Carrier ProteinsAntineoplastic AgentsMESH: Protein-Tyrosine KinasesMESH: Protein-Serine-Threonine KinasesMESH : Cisplatin03 medical and health sciencesMESH: Cell Cycle ProteinsGenotoxic stressMESH : Protein-Tyrosine KinasesHumansMESH : HistonesAnticancer TherapyMESH: DNA DamageCisplatinMESH: HumansMESH: Phosphorylation[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH : HumansMESH : Nuclear Proteins030104 developmental biologyCancer cellMESH: Antineoplastic AgentsCisplatinCarrier ProteinsMESH: Nuclear ProteinsMESH : ApoptosisDna-damage response0301 basic medicineCancer ResearchMESH: Caspase 3MESH : Caspase 3PhosphorylationCytotoxicityMESH : DNA DamageSensitizationmedicine.diagnostic_testCaspase 3Nuclear ProteinsProtein-Tyrosine KinasesMESH : Survival RateMitochondriaG2 Phase Cell Cycle CheckpointsWee1medicine.anatomical_structureMESH : Protein Phosphatase 2COriginal ArticleMESH : MitochondriaColorectal Neoplasmsmedicine.drugMESH : Protein-Serine-Threonine KinasesMESH: Cell Line TumorMESH: Survival RateMESH: Mice TransgenicMESH: RNA InterferencePhosphataseMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesFlow cytometryCellular and Molecular NeuroscienceCell Line TumorMESH : MicemedicineAnimalsMESH: MiceMESH : Cell Line TumorMESH: ApoptosisCell BiologyMESH : Tumor Suppressor Protein p53MESH: CisplatinCancer researchbiology.proteinMESH : AnimalsMESH : G2 Phase Cell Cycle CheckpointsMESH : RNA InterferenceTumor Suppressor Protein p53MESH: Colorectal NeoplasmsDNA DamageCell Death & Disease
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