Search results for "Xenograft Model Antitumor Assay"

showing 10 items of 132 documents

Imatinib spares cKit-expressing prostate neuroendocrine tumors, whereas kills seminal vesicle epithelial-stromal tumors by targeting PDGFR-β

2017

Abstract Prostate cancer is a leading cause of cancer-related death in males worldwide. Indeed, advanced and metastatic disease characterized by androgen resistance and often associated with neuroendocrine (NE) differentiation remains incurable. Using the spontaneous prostate cancer TRAMP model, we have shown that mast cells (MCs) support in vivo the growth of prostate adenocarcinoma, whereas their genetic or pharmacologic targeting favors prostate NE cancer arousal. Aiming at simultaneously targeting prostate NE tumor cells and MCs, both expressing the cKit tyrosine kinase receptor, we have tested the therapeutic effect of imatinib in TRAMP mice. Imatinib-treated TRAMP mice experience a pa…

0301 basic medicineMaleCancer ResearchReceptor tyrosine kinaseAntineoplastic AgentProstate cancerMice0302 clinical medicineProstatebiologySeminal VesiclesImmunohistochemistryGene Expression Regulation NeoplasticNeuroendocrine TumorsProto-Oncogene Proteins c-kitmedicine.anatomical_structureOncology030220 oncology & carcinogenesisImatinib MesylateFemaleNeuroendocrine Tumormedicine.drugTrampHumanSignal TransductionPCA3medicine.medical_specialtyStromal cellXenograft Model Antitumor AssayProtein Kinase InhibitorAntineoplastic AgentsMice TransgenicReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesInternal medicineSeminal VesiclemedicineAnimalsHumansProtein Kinase InhibitorsAnimalProstatic NeoplasmsImatinibBiomarkermedicine.diseaseXenograft Model Antitumor AssaysDisease Models Animal030104 developmental biologyEndocrinologyImatinib mesylateProstatic Neoplasmbiology.proteinCancer researchBiomarkers
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LXR agonist treatment of blastic plasmacytoid dendritic cell neoplasm restores cholesterol efflux and triggers apoptosis

2016

International audience; Blastic plasmacytoid dendritic cell (PDC) neoplasm (BPDCN) is an aggressive hematological malignancy with a poor prognosis that derives from PDCs. No consensus for optimal treatment modalities is available today and the full characterization of this leukemia is still emerging. We identified here a BPDCN-specific transcriptomic profile when compared with those of acute myeloid leukemia and T-acute lymphoblastic leukemia, as well as the transcriptomic signature of primary PDCs. This BPDCN gene signature identified a dysregulation of genes involved in cholesterol homeostasis, some of them being liver X receptor (LXR) target genes. LXR agonist treatment of primary BPDCN …

0301 basic medicineMaleCellProliferationApoptosisExpressionPlasmacytoid dendritic cellPrecursor T-Cell Lymphoblastic Leukemia-LymphomaBiochemistryMice0302 clinical medicinepolycyclic compoundsSTAT5 Transcription Factor[ SDV.MHEP.HEM ] Life Sciences [q-bio]/Human health and pathology/HematologyATP Binding Cassette Transporter Subfamily G Member 1Liver X ReceptorsInhibitionMyeloid NeoplasiabiologyMyeloid leukemiafood and beveragesMyeloid-Leukemia[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyHematologyInterleukin-3 Receptor3. Good healthLeukemiamedicine.anatomical_structureCholesterol030220 oncology & carcinogenesisFemalelipids (amino acids peptides and proteins)In-VivoATP Binding Cassette Transporter 1ImmunologyActivationAntineoplastic Agentsdigestive system03 medical and health sciencesCell Line TumormedicineAnimalsHumansLiver X receptorProtein kinase BCell ProliferationCell growthCell BiologyDendritic Cellsmedicine.diseaseXenograft Model Antitumor Assays030104 developmental biologyProstate-Cancer CellsABCA1biology.proteinCancer researchDensity-Lipoprotein ReceptorInterleukin-3Proto-Oncogene Proteins c-akt
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Moving Towards Precision Urologic Oncology: Targeting Enzalutamide-resistant Prostate Cancer and Mutated Forms of the Androgen Receptor Using the Nov…

2017

Abstract Darolutamide (ODM-201) is a novel androgen receptor (AR) antagonist with a chemical structure distinctly different from currently approved AR antagonists that targets both wild-type and mutated ligand binding domain variants to inhibit AR nuclear translocation. Here, we evaluate the activity of darolutamide in enzalutamide-resistant castration resistant prostate cancer (CRPC) as well as in AR mutants detected in patients after treatment with enzalutamide, abiraterone, or bicalutamide. Darolutamide significantly inhibited cell growth and AR transcriptional activity in enzalutamide-resistant MR49F cells in vitro, and led to decreased tumor volume and serum prostate-specific antigen l…

0301 basic medicineMaleModels MolecularTime FactorsTranscription GeneticProtein ConformationProstate cancerchemistry.chemical_compoundMice0302 clinical medicineMolecular Targeted TherapyTumor BurdenDarolutamideReceptors Androgen030220 oncology & carcinogenesisBenzamidesmedicine.drugSignal Transductionmedicine.medical_specialtyBicalutamideUrologyPartial agonist03 medical and health sciencesStructure-Activity RelationshipIn vivoInternal medicineCell Line TumorNitrilesPhenylthiohydantoinmedicineAndrogen Receptor AntagonistsEnzalutamideAnimalsHumansCell ProliferationDose-Response Relationship DrugCell growthbusiness.industryProstatic Neoplasmsmedicine.diseaseXenograft Model Antitumor AssaysAndrogen receptor030104 developmental biologyEndocrinologychemistryDrug Resistance NeoplasmMutationCancer researchPyrazolesbusinessEuropean urology
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A 13 mer LNA-i-miR-221 Inhibitor Restores Drug Sensitivity in Melphalan-Refractory Multiple Myeloma Cells.

2016

Abstract Purpose: The onset of drug resistance is a major cause of treatment failure in multiple myeloma. Although increasing evidence is defining the role of miRNAs in mediating drug resistance, their potential activity as drug-sensitizing agents has not yet been investigated in multiple myeloma. Experimental Design: Here we studied the potential utility of miR-221/222 inhibition in sensitizing refractory multiple myeloma cells to melphalan. Results: miR-221/222 expression inversely correlated with melphalan sensitivity of multiple myeloma cells. Inhibition of miR-221/222 overcame melphalan resistance and triggered apoptosis of multiple myeloma cells in vitro, in the presence or absence of…

0301 basic medicineMelphalanCancer ResearchStromal cellApoptosisDrug resistancePharmacologyArticle03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicinemyeloma microRNA mir-221 melphalanimmune system diseasesIn vivohemic and lymphatic diseasesCell Line TumorProto-Oncogene ProteinsmedicineAnimalsHumansMelphalanMultiple myelomaNOD miceCell Proliferationbusiness.industryCancermedicine.diseaseXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologyOncologychemistryDrug Resistance Neoplasm030220 oncology & carcinogenesisGrowth inhibitionMultidrug Resistance-Associated ProteinsbusinessApoptosis Regulatory ProteinsMultiple Myelomamedicine.drugClinical cancer research : an official journal of the American Association for Cancer Research
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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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Antibody-mediated blockade of JMJD6 interaction with collagen I exerts antifibrotic and antimetastatic activities

2017

JMJD6 is known to localize in the nucleus, exerting histone arginine demethylase and lysyl hydroxylase activities. A novel localization of JMJD6 in the extracellular matrix, resulting from its secretion as a soluble protein, was unveiled by a new anti-JMJD6 mAb called P4E11, which was developed to identify new targets in the stroma. Recombinant JMJD6 binds with collagen type I (Coll-I), and distinct JMJD6 peptides interfere with collagen fibrillogenesis, collagen-fibronectin interaction, and adhesion of human tumor cells to the collagen substrate. P4E11 and collagen binding to JMJD6 are mutually exclusive because the amino acid sequences of JMJD6 necessary for the interaction with Coll-I ar…

0301 basic medicineMonoclonal antibodyXenograft Model Antitumor AssayArginineLysyl hydroxylaseEnzyme-Linked Immunosorbent AssayReceptors Cell SurfacePlasma protein bindingBiochemistryCollagen Type IExtracellular matrix03 medical and health sciencesMiceFibrosisPeptide LibraryCell Line TumormedicineGeneticsAnimalsHumansOsteonectinCell NucleuMolecular BiologyCell NucleusMice KnockoutMice Inbred BALB CbiologyChemistryJmjC familyAnimalAntibodies MonoclonalFibrillogenesisExtracellular matrixmedicine.diseaseXenograft Model Antitumor AssaysImmunohistochemistryCell biologyIn vivo treatment030104 developmental biologybiology.proteinOsteonectinSignal transductionExtracellular matrix; In vivo treatment; JmjC family; Monoclonal antibody; Peptide library; Animals; Antibodies Monoclonal; Cell Line Tumor; Cell Nucleus; Collagen Type I; Enzyme-Linked Immunosorbent Assay; Extracellular Matrix; Humans; Immunohistochemistry; Mice; Mice Inbred BALB C; Mice Knockout; Osteonectin; Peptide Library; Protein Binding; Receptors Cell Surface; Signal Transduction; Xenograft Model Antitumor Assays; Biotechnology; Biochemistry; Molecular Biology; GeneticsHumanProtein BindingSignal TransductionBiotechnology
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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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TEM8/ANTXR1-Specific CAR T Cells as a Targeted Therapy for Triple-Negative Breast Cancer.

2018

Abstract Triple-negative breast cancer (TNBC) is an aggressive disease lacking targeted therapy. In this study, we developed a CAR T cell–based immunotherapeutic strategy to target TEM8, a marker initially defined on endothelial cells in colon tumors that was discovered recently to be upregulated in TNBC. CAR T cells were developed that upon specific recognition of TEM8 secreted immunostimulatory cytokines and killed tumor endothelial cells as well as TEM8-positive TNBC cells. Notably, the TEM8 CAR T cells targeted breast cancer stem–like cells, offsetting the formation of mammospheres relative to nontransduced T cells. Adoptive transfer of TEM8 CAR T cells induced regression of established…

0301 basic medicineOncologyCancer ResearchAdoptive cell transfermedicine.medical_specialtyLung Neoplasmsmedicine.medical_treatmentT-LymphocytesCell- and Tissue-Based TherapyReceptors Antigen T-CellApoptosisReceptors Cell SurfaceTriple Negative Breast NeoplasmsTargeted therapy03 medical and health sciencesMice0302 clinical medicineBreast cancerAntigenInternal medicineBiomarkers TumorTumor Cells CulturedMedicineAnimalsHumansTriple-negative breast cancerCell Proliferationbusiness.industryMicrofilament ProteinsCancerImmunotherapyTriple Negative Breast Neoplasmsmedicine.diseasePrognosisXenograft Model Antitumor AssaysNeoplasm ProteinsSurvival Rate030104 developmental biologyOncology030220 oncology & carcinogenesisCase-Control StudiesFemaleImmunotherapybusinessFollow-Up StudiesCancer research
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Patient-derived solitary fibrous tumour xenografts predict high sensitivity to doxorubicin/dacarbazine combination confirmed in the clinic and highli…

2017

Abstract Background Preclinical models that mimic pathological and molecular features of solitary fibrous tumour (SFT) represent an important tool to select effective regimes and novel compounds to be tested in the clinic. This study was aimed at developing two preclinical models of SFT, assessing their predictive value in the clinic and selecting potential novel effective treatments. Material and methods Two dedifferentiated-SFT (D-SFT) models obtained from patients' biopsies were grown in immunodeficient mice. The antitumour activity on these models of doxorubicin, dacarbazine (DTIC), ifosfamide (monotherapy or combination), trabectedin and eribulin was tested. Twelve SFT patients were tr…

0301 basic medicineOncologyMaleCancer Researchmedicine.medical_treatmentSolitary fibrous tumourSoft Tissue NeoplasmsDioxoleMice SCIDPharmacologyAnthracyclineMetastasichemistry.chemical_compound0302 clinical medicineSolitary Fibrous TumorRetrospective StudieTetrahydroisoquinolinesAntineoplastic Combined Chemotherapy ProtocolsTetrahydroisoquinolineMeningeal NeoplasmsMeningeal NeoplasmPleural NeoplasmTrabectedinIfosfamideKidney NeoplasmSarcomaKetonesMiddle AgedMice modelKetoneKidney NeoplasmsDacarbazineSurvival RateOncologyResponse Evaluation Criteria in Solid TumorsSolitary Fibrous Tumors030220 oncology & carcinogenesisFemalemedicine.drugEribulinHumanAdultmedicine.medical_specialtyXenograft Model Antitumor AssayAnthracyclinePleural NeoplasmsDacarbazineBlotting WesternResponse Evaluation Criteria in Solid TumorDioxolesDisease-Free Survival03 medical and health sciencesInternal medicinemedicineAnimalsHumansChemotherapyFuranDoxorubicinRetroperitoneal NeoplasmsEribulinIfosfamideSoft Tissue NeoplasmCerebellar NeoplasmsFuransResponse Evaluation Criteria in Solid TumorsRetrospective StudiesAgedChemotherapyAntineoplastic Combined Chemotherapy ProtocolRetroperitoneal Neoplasmbusiness.industryAnimalXenograftCerebellar NeoplasmXenograft Model Antitumor AssaysTreatment030104 developmental biologychemistryDoxorubicinbusinessTrabectedin
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CIMT 2018: Pushing frontiers in cancer immunotherapy — Report on the 16th Annual Meeting of the Association for Cancer Immunotherapy

2018

ABSTRACT The 16th Annual Meeting of the Association for Cancer Immunotherapy (CIMT), Europe’s largest meeting series of its kind, took place in Mainz, Germany from 15–17 May, 2018. Cutting-edge advancements in cancer immunotherapy were discussed among more than 700 scientists under the motto “Pushing Frontiers in Cancer Immunotherapy”. This meeting report is a summary of some of the CIMT 2018 highlights.

0301 basic medicineOncologymedicine.medical_specialtyCombination therapymedicine.medical_treatmentImmunologyMeeting Reportcombination therapyCell therapy03 medical and health sciencesCancer immunotherapyInternal medicineNeoplasmsmedicineTumor MicroenvironmentImmunology and AllergyAnimalsHumansPersonalized therapytumor vaccinationPharmacologypersonalized therapyTumor microenvironmentcancer immunotherapybusiness.industryVaccinationCIMTcellular therapyCongresses as TopicXenograft Model Antitumor AssaysDisease Models Animal030104 developmental biologycheckpoint blockadeDrug Therapy CombinationImmunotherapybusinessHuman Vaccines & Immunotherapeutics
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