Search results for "antineoplastic agent"

showing 10 items of 1538 documents

Retrospective Analysis of Checkpoint Inhibitor Therapy-Associated Cases of Bullous Pemphigoid From Six German Dermatology Centers

2021

Immune-related adverse events (irAEs) are a class-effect of checkpoint inhibitors (CIs). The development of a Bullous pemphigoid (BP)-like blistering disease, driven by autoantibodies against the hemidesmosomal protein BP180, is a potentially serious irAE whose incidence seems to be increasing. We therefore set out to characterize the clinical and (immuno)histopathological features and treatment responses of cases of BP which developed during or after CI therapy collated in six German tertiary referral centers between 2014 and 2018. We identified twelve cases of BP which emerged during and/or after CI therapy. The time interval between the initiation of CI therapy and the diagnosis of BP wa…

0301 basic medicineMalelcsh:Immunologic diseases. Allergymedicine.medical_specialtyPD-1 - PD-L1 axisautoantibodiesImmune checkpoint inhibitorsImmunologypemphigoid diseaseIpilimumabPembrolizumabDermatology030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicineAntineoplastic Agents ImmunologicalAdrenal Cortex HormonesInternal medicineGermanyNeoplasmsPemphigoid BullousmedicineHumansImmunology and AllergyipilimumabAdverse effectImmune Checkpoint InhibitorsAgedRetrospective StudiesOriginal ResearchAged 80 and overnivolumabbusiness.industryIncidence (epidemiology)autoimmunityAutoantibodyMiddle Agedmedicine.disease030104 developmental biologyFemaleBullous pemphigoidpembrolizumabNivolumabbusinesslcsh:RC581-607checkpoint inhibitorsmedicine.drugFrontiers in Immunology
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EGFL7 enhances surface expression of integrin α5β1 to promote angiogenesis in malignant brain tumors

2018

Abstract Glioblastoma (GBM) is a typically lethal type of brain tumor with a median survival of 15 months postdiagnosis. This negative prognosis prompted the exploration of alternative treatment options. In particular, the reliance of GBM on angiogenesis triggered the development of anti‐VEGF (vascular endothelial growth factor) blocking antibodies such as bevacizumab. Although its application in human GBM only increased progression‐free periods but did not improve overall survival, physicians and researchers still utilize this treatment option due to the lack of adequate alternatives. In an attempt to improve the efficacy of anti‐VEGF treatment, we explored the role of the egfl7 gene in ma…

0301 basic medicineMedicine (General)Vascular Biology & AngiogenesisAngiogenesisEndothelial Growth FactorsQH426-470chemistry.chemical_compoundangiogenesisMice0302 clinical medicineAntineoplastic Agents ImmunologicalResearch ArticlesCancerNeovascularization PathologicBrain NeoplasmsEndothelial stem cellVascular endothelial growth factormedicine.anatomical_structureTreatment Outcome030220 oncology & carcinogenesisendothelial cellMolecular MedicineHeterograftsEGFL7PericyteEGFL7medicine.drugResearch ArticleIntegrin alpha5beta1EGF Family of ProteinsintegrinBrain tumor03 medical and health sciencesR5-920GliomamedicineGeneticsHuman Umbilical Vein Endothelial CellsAnimalsHumansddc:610Cell ProliferationTemozolomidebusiness.industryCalcium-Binding ProteinsglioblastomaEndothelial Cellsmedicine.diseaseSurvival AnalysisDisease Models Animal030104 developmental biologychemistryCancer researchbusinessNeoplasm TransplantationNeuroscienceEMBO Molecular Medicine
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Interleukin 3- receptor targeted exosomes inhibit in vitro and in vivo chronic myelogenous Leukemia cell growth

2017

Despite Imatinib (IM), a selective inhibitor of Bcr-Abl, having led to improved prognosis in Chronic Myeloid Leukemia (CML) patients, acquired resistance and long-term adverse effects is still being encountered. There is, therefore, urgent need to develop alternative strategies to overcome drug resistance. According to the molecules expressed on their surface, exosomes can target specific cells. Exosomes can also be loaded with a variety of molecules, thereby acting as a vehicle for the delivery of therapeutic agents. In this study, we engineered HEK293T cells to express the exosomal protein Lamp2b, fused to a fragment of Interleukin 3 (IL3). The IL3 receptor (IL3-R) is overexpressed in CML…

0301 basic medicineMedicine (miscellaneous)PharmacologyEngineered exosomeExosomesInterleukin 3Antineoplastic AgentMiceHEK293 Cellhemic and lymphatic diseasesDrug CarrierPharmacology Toxicology and Pharmaceutics (miscellaneous)Drug CarriersChronic myeloid leukemiaMyeloid leukemiaChronic myeloid leukemia; Drug delivery; Drug resistance; Engineered exosomes; Interleukin 3; Animals; Antineoplastic Agents; Cell Line Tumor; Cell Proliferation; Disease Models Animal; Drug Carriers; Exosomes; HEK293 Cells; Heterografts; Humans; Imatinib Mesylate; Leukemia Myelogenous Chronic BCR-ABL Positive; Mice; Receptors Interleukin-3; Treatment Outcome3. Good healthTreatment OutcomeImatinib MesylateHeterograftsHeterograftResearch Papermedicine.drugHumanEngineered exosomesAntineoplastic Agents03 medical and health sciencesIn vivoCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineAnimalsHumansneoplasmsInterleukin 3.Interleukin 3Cell Proliferationbusiness.industryAnimalImatinibmedicine.diseaseMicrovesiclesReceptors Interleukin-3ExosomeDisease Models AnimalHEK293 Cells030104 developmental biologyImatinib mesylateDrug resistanceCancer cellDrug deliverybusinessChronic myelogenous leukemia
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Enhanced emergence of antibiotic-resistant pathogenic bacteria after in vitro induction with cancer chemotherapy drugs.

2019

International audience; BACKGROUND:Infections with antibiotic-resistant pathogens in cancer patients are a leading cause of mortality. Cancer patients are treated with compounds that can damage bacterial DNA, potentially triggering the SOS response, which in turn enhances the bacterial mutation rate. Antibiotic resistance readily occurs after mutation of bacterial core genes. Thus, we tested whether cancer chemotherapy drugs enhance the emergence of resistant mutants in commensal bacteria.METHODS:Induction of the SOS response was tested after the incubation of Escherichia coli biosensors with 39 chemotherapeutic drugs at therapeutic concentrations. The mutation frequency was assessed after …

0301 basic medicineMicrobiology (medical)Staphylococcus aureusmedicine.drug_class030106 microbiologyAntibioticsAntineoplastic AgentsDrug resistanceMicrobial Sensitivity TestsBiologymedicine.disease_causeMicrobiology03 medical and health sciencesSOS Response (Genetics)0302 clinical medicineAntibiotic resistanceDrug Resistance BacterialEnterobacter cloacaemedicineHumansPharmacology (medical)030212 general & internal medicineMutation frequencySOS responseSOS Response GeneticsPharmacologyPathogenic bacteriaChemotherapy regimen3. Good healthAnti-Bacterial Agents[SDV.MP]Life Sciences [q-bio]/Microbiology and ParasitologyInfectious DiseasesPseudomonas aeruginosaThe Journal of antimicrobial chemotherapy
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Oncogenic Deregulation of EZH2 as an Opportunity for Targeted Therapy in Lung Cancer.

2016

Abstract As a master regulator of chromatin function, the lysine methyltransferase EZH2 orchestrates transcriptional silencing of developmental gene networks. Overexpression of EZH2 is commonly observed in human epithelial cancers, such as non–small cell lung carcinoma (NSCLC), yet definitive demonstration of malignant transformation by deregulated EZH2 remains elusive. Here, we demonstrate the causal role of EZH2 overexpression in NSCLC with new genetically engineered mouse models of lung adenocarcinoma. Deregulated EZH2 silences normal developmental pathways, leading to epigenetic transformation independent of canonical growth factor pathway activation. As such, tumors feature a transcrip…

0301 basic medicineModels MolecularLung Neoplasmsmedicine.medical_treatmentMolecular ConformationGene ExpressionAntineoplastic Agentsmacromolecular substancesBiologymedicine.disease_causeArticleMalignant transformationTargeted therapy03 medical and health sciencesMiceStructure-Activity RelationshipCell Line TumormedicineAnimalsHumansEnhancer of Zeste Homolog 2 ProteinMolecular Targeted TherapyLung cancerPromoter Regions GeneticGene Expression ProfilingEZH2Cancermedicine.diseaseMagnetic Resonance ImagingXenograft Model Antitumor AssaysChromatinrespiratory tract diseasesGene Expression Regulation NeoplasticDisease Models Animal030104 developmental biologyCell Transformation NeoplasticEnhancer Elements GeneticOncologyDrug DesignCancer researchAdenocarcinomaKRASEpigenetic therapyCancer discovery
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1,3,5-Triazines: A promising scaffold for anticancer drugs development

2017

This review covering literature reports from the beginning of this century to 2016 describes the synthetic pathways, the antitumor activity, the structure-activity relationship and, whenever reported, the possible mechanism of action of 1,3,5-triazine derivatives as well as of their hetero-fused compounds. Many 1,3,5-triazine derivatives, both uncondensed and hetero-fused, have shown remarkable antitumor activities and some of them reached clinical development.

0301 basic medicineModels MolecularScaffold31Disubstituted 135-triazineTrisubstituted 135-triazineAntineoplastic AgentsChemistry Techniques Synthetic01 natural sciences03 medical and health sciencesStructure-Activity RelationshipNeoplasmsDrug DiscoverymedicineAnimalsHumans5-TriazinesTrisubstituted 1Disubstituted 1Antitumor activityPharmacologyHeterofused 135-triazine010405 organic chemistryChemistryTriazinesNitrogen heterocyclesDrug Discovery3003 Pharmaceutical ScienceOrganic ChemistryGeneral MedicineHeterofused 1Combinatorial chemistry135-Triazine0104 chemical sciences030104 developmental biologyNitrogen heterocycleMechanism of action1; 3; 5-Triazines; Antitumor activity; Disubstituted 1; 3; 5-triazines; Heterofused 1; 3; 5-triazines; Nitrogen heterocycles; Trisubstituted 1; 3; 5-triazines; Pharmacology; Drug Discovery3003 Pharmaceutical Science; Organic Chemistrymedicine.symptomAntitumor activity
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Investigation on Quantitative Structure-Activity Relationships of 1,3,4-Oxadiazole Derivatives as Potential Telomerase Inhibitors.

2020

Background:Telomerase, a reverse transcriptase, maintains telomere and chromosomes integrity of dividing cells, while it is inactivated in most somatic cells. In tumor cells, telomerase is highly activated, and works in order to maintain the length of telomeres causing immortality, hence it could be considered as a potential marker to tumorigenesis.A series of 1,3,4-oxadiazole derivatives showed significant broad-spectrum anticancer activity against different cell lines, and demonstrated telomerase inhibition.Methods:This series of 24 N-benzylidene-2-((5-(pyridine-4-yl)-1,3,4-oxadiazol-2yl)thio)acetohydrazide derivatives as telomerase inhibitors has been considered to carry out QSAR studies…

0301 basic medicineModels MolecularTelomeraseQuantitative structure–activity relationship2D descriptorsDatasets as TopicQuantitative Structure-Activity RelationshipAntineoplastic Agents010402 general chemistry01 natural sciencesModels BiologicalAnticancer activityMLR03 medical and health sciencesInhibitory Concentration 50Drug DiscoveryLeast-Squares AnalysisTelomerase134-oxadiazolesOxadiazolesMolecular StructureDrug discoveryChemistryQSARQuantitative structureCombinatorial chemistry0104 chemical sciencesTelomerase inhibitors030104 developmental biology1 3 4 oxadiazole derivativesDrug Screening Assays AntitumorCurrent drug discovery technologies
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Immunmodulatory and Antiproliferative Properties of Rhodiola Species.

2016

The traditional medicines of Asia and Europe have long used various Rhodiola species, which are endemic to the subarctic areas of the northern hemisphere, as tonic, adaptogen, antidepressant, and anti-inflammatory drugs. In order to establish the therapeutic uses of these plants in modern medicine, the pharmacological effects of Rhodiola sp. have been widely studied. Indeed, the most amply researched species, Rhodiola rosea, has been shown to possess antioxidant, adaptogenic, antistress, antimicrobial, immunomodulatory, angiomodulatory, and antitumoral effects. Salidroside (p-hydroxyphenethyl-β-D-glucoside), a major compound in Rhodiola, seems to be responsible for many of the effects obser…

0301 basic medicineModern medicineRhodiola algidaImmunologic Factorsmedicine.medical_treatmentPharmaceutical SciencePharmacologyAnalytical Chemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineGlucosidesPhenolsSpecies SpecificityDrug DiscoveryAdaptogenRhodiolamedicineAnimalsHumansImmunologic FactorsRhodiola crenulataCell ProliferationPharmacologybiologyTraditional medicinePlant ExtractsOrganic ChemistrySalidrosidebiology.organism_classificationAntineoplastic Agents Phytogenic030104 developmental biologyRhodiola roseaComplementary and alternative medicinechemistry030220 oncology & carcinogenesisMolecular MedicineRhodiolaPlanta medica
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Identification of the Privileged Position in the Imidazo[1,2-a]pyridine Ring of Phosphonocarboxylates for Development of Rab Geranylgeranyl Transfera…

2017

Members of the Rab GTPase family are master regulators of vesicle trafficking. When disregulated, they are associated with a number of pathological states. The inhibition of RGGT, an enzyme responsible for post-translational geranylgeranylation of Rab GTPases represents one way to control the activity of these proteins. Because the number of molecules modulating RGGT is limited, we combined molecular modeling with biological assays to ascertain how modifications of phosphonocarboxylates, the first reported RGGT inhibitors, rationally improve understanding of their structure-activity relationship. We have identified the privileged position in the core scaffold of the imidazo[1,2-a]pyridine r…

0301 basic medicineMolecular modelPyridinesOrganophosphonatesProtein PrenylationAntineoplastic AgentsGTPase01 natural sciencesHeLa03 medical and health sciencesStructure-Activity RelationshipGeranylgeranylationPrenylationDrug DiscoveryStructure–activity relationshipHumansEnzyme Inhibitorsta116Cell Proliferationchemistry.chemical_classificationAlkyl and Aryl Transferasesbiology010405 organic chemistryrab geranylgeranyl transferaseta1182biology.organism_classification0104 chemical sciencesCell biologyMolecular Docking Simulation030104 developmental biologyEnzymechemistryBiochemistryrab GTP-Binding ProteinsMolecular MedicineRabHeLa CellsJournal of Medicinal Chemistry
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Mesenchymal Transition of High-Grade Breast Carcinomas Depends on Extracellular Matrix Control of Myeloid Suppressor Cell Activity

2016

SummaryThe extracellular matrix (ECM) contributes to the biological and clinical heterogeneity of breast cancer, and different prognostic groups can be identified according to specific ECM signatures. In high-grade, but not low-grade, tumors, an ECM signature characterized by high SPARC expression (ECM3) identifies tumors with increased epithelial-to-mesenchymal transition (EMT), reduced treatment response, and poor prognosis. To better understand how this ECM3 signature is contributing to tumorigenesis, we expressed SPARC in isogenic cell lines and found that SPARC overexpression in tumor cells reduces their growth rate and induces EMT. SPARC expression also results in the formation of a h…

0301 basic medicineMyeloidMDSCGene Expressionmedicine.disease_causeT-Lymphocytes RegulatoryPolyethylene GlycolsExtracellular matrixMiceBreast cancerMyeloid CellsOsteonectinMast Cellslcsh:QH301-705.5Mice KnockoutAntigen PresentationMice Inbred BALB CEMTepithelial to mesenchymal transitionBreast cancer; COX-2; CXCL12; ECM; EMT; G-CSF; GM-CSF; MDSC; SPARC; aminobisphosphonates; cyclooxygenase-2; epithelial to mesenchymal transition; extracellular matrix; granulocyte colony-stimulating factor; granulocyte-macrophage colony-stimulating factor; myeloid-derived suppressor cellsCXCL12Granulocyte macrophage colony-stimulating factormedicine.anatomical_structurecyclooxygenase-2granulocyte-macrophage colony-stimulating factorFemalegranulocyte colony-stimulating factormedicine.drugEpithelial-Mesenchymal Transitionextracellular matrixAntineoplastic AgentsBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaG-CSFGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpithelial–mesenchymal transitionECMMesenchymal stem cellSPARCGM-CSFCOX-2myeloid-derived suppressor cellsXenograft Model Antitumor AssaysIsogenic human disease modelsaminobisphosphonates030104 developmental biologylcsh:Biology (General)CelecoxibDoxorubicinImmunologyCancer researchMyeloid-derived Suppressor CellaminobisphosphonateNeoplasm GradingCarcinogenesisCell Reports
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