Search results for "XENOGRAFT"

showing 10 items of 161 documents

Targeting the Cancer Initiating Cell: The Ultimate Target for Cancer Therapy

2012

An area of therapeutic interest in cancer biology and treatment is targeting the cancer stem cell, more appropriately referred to as the cancer initiating cell (CIC). CICs comprise a subset of hierarchically organized, rare cancer cells with the ability to initiate cancer in xenografts in genetically modified murine models. CICs are thought to be responsible for tumor onset, self-renewal/maintenance, mutation accumulation and metastasis. CICs may lay dormant after various cancer therapies which eliminate the more rapidly proliferating bulk cancer (BC) mass. However, CICs may remerge after therapy is discontinued as they may represent cells which were either intrinsically resistant to the or…

PTENgerminal mutationchemotherapeuticmedicine.medical_treatmentAntineoplastic AgentsPI3KTargeted therapyMetastasisMice03 medical and health sciencesTARGETED THERAPY0302 clinical medicineCancer stem cellNeoplasmsradiologicalDrug DiscoverymedicineAnimalsHumansPTENAkt; mTOR; PI3K; PTEN; Targeted therapy; Therapeutic sensitivityPI3K/AKT/mTOR pathway030304 developmental biologyPharmacologyBiological Products0303 health sciencesbiologyAKTMTORAktCD44Wnt signaling pathwayCancertargeted therapymedicine.disease3. Good healththerapeutic sensitivityxenografts030220 oncology & carcinogenesisImmunologymTORNeoplastic Stem CellsCancer researchbiology.proteinCurrent Pharmaceutical Design
researchProduct

Endothelial Wnt/β-catenin signaling inhibits glioma angiogenesis and normalizes tumor blood vessels by inducing PDGF-B expression

2012

Wnt modulates glioma vascularization by regulating PDGF-B expression.

PathologyAngiogenesisCentral Nervous System NeoplasmsMice0302 clinical medicineImmunology and AllergyWnt Signaling Pathwaybeta Catenin0303 health sciencesbiologyNeovascularization PathologicBrain NeoplasmsWnt signaling pathwayIntracellular Signaling Peptides and ProteinsForkhead Transcription FactorsGliomaProto-Oncogene Proteins c-sis3. Good healthmedicine.anatomical_structureBlood-Brain Barrier030220 oncology & carcinogenesiscardiovascular systemIntercellular Signaling Peptides and ProteinsFemalemedicine.medical_specialtyBeta-cateninEndotheliumImmunologyNotch signaling pathwayMice NudeWnt1 ProteinMural cellArticle03 medical and health sciencesGliomamedicineAnimalsHumansddc:610neoplasms030304 developmental biologyAdaptor Proteins Signal TransducingCalcium-Binding ProteinsMembrane Proteinsmedicine.diseaseXenograft Model Antitumor Assaysnervous system diseasesDKK1Cancer researchbiology.proteinEndothelium VascularNeoplasm Grading
researchProduct

MMP-13 stimulates osteoclast differentiation and activation in tumour breast bone metastases

2011

INTRODUCTION: The increased bone degradation in osteolytic metastases depends on stimulation of mature osteoclasts and on continuous differentiation of new pre-osteoclasts. Metalloproteinases (MMP)-13 is expressed in a broad range of primary malignant tumours and it is emerging as a novel biomarker. Recent data suggest a direct role of MMP-13 in dissolving bone matrix complementing the activity of MMP-9 and other enzymes. Tumour-microenvironment interactions alter gene expression in malignant breast tumour cells promoting osteolytic bone metastasis. Gene expression profiles revealed that MMP-13 was among the up-regulated genes in tumour-bone interface and its abrogation reduced bone erosion…

Pathologymedicine.medical_specialtyCellular differentiationGalectin 3Mice NudeOsteoclastsBone NeoplasmsBreast NeoplasmsMatrix metalloproteinaseAdenocarcinomaExtracellular matrixMiceOsteoclastCell Line TumorMatrix Metalloproteinase 13medicineAnimalsHumansProtein PrecursorsOSTEOCLASTMedicine(all)MMP13 ; OSTEOCLAST; BREAST TUMORChemistryMMP13Bone metastasisCell Differentiationmedicine.diseaseXenograft Model Antitumor AssaysResorptionExtracellular Matrixmedicine.anatomical_structureCellular MicroenvironmentMatrix Metalloproteinase 9Galectin-3Cancer researchCytokinesFemaleBone marrowBREAST TUMORResearch ArticleBreast Cancer Research : BCR
researchProduct

Targeting of multiple myeloma-related angiogenesis by miR-199a-5p mimics: in vitro and in vivo anti-tumor activity

2014

// Lavinia Raimondi 1 , Nicola Amodio 1 , Maria Teresa Di Martino 1 , Emanuela Altomare 1 , Marzia Leotta 1 , Daniele Caracciolo 1 , Annamaria Gulla 1 , Antonino Neri 2 , Simona Taverna 3 , Patrizia D’Aquila 4 , Riccardo Alessandro 3 , Antonio Giordano 5 , Pierosandro Tagliaferri 1 and Pierfrancesco Tassone 1,5 . 1 Department of Experimental and Clinical Medicine, Magna Graecia University and Medical Oncology Unit, T. Campanella Cancer Center, Salvatore Venuta University Campus, Catanzaro, Italy 2 Department of Medical Sciences University of Milan, Hematology1, IRCCS Policlinico Foundation, Milan, Italy 3 Department of Pathology and Forensic and Medical Biotechnology, Section of Biology and…

Pathologymedicine.medical_specialtyStromal cellAngiogenesisMultiple Myeloma; microRNA AngiogenesisBlotting WesternEnzyme-Linked Immunosorbent AssayMice SCIDIn Vitro TechniquesBiologyReal-Time Polymerase Chain ReactionTransfectionMicemiR-199-5pCell MovementMice Inbred NODSettore BIO/13 - Biologia ApplicataCell Line TumorCell AdhesionmedicineAnimalsHumansHypoxiaCell adhesionProtein kinase BCell ProliferationPlasma cell leukemiaNeovascularization PathologicmicroRNA AngiogenesisMicroRNATransfectionPlasma cell leukemiamedicine.diseaseXenograft Model Antitumor AssaysMolecular medicineCell HypoxiaMicroRNAsmedicine.anatomical_structureOncologyAngiogenesis; Hypoxia; Microenviroment; MicroRNA; miR-199-5p; MiRNA; Multiple myeloma; Plasma cell leukemiaCancer researchFemaleAngiogenesisBone marrowMicroenviromentMiRNAMultiple MyelomaResearch Paper
researchProduct

Human bone marrow mesenchymal stem cells display anti-cancer activity in SCID mice bearing disseminated non-Hodgkin's lymphoma xenografts.

2010

Background Although multimodality treatment can induce high rate of remission in many subtypes of non-Hodgkin's lymphoma (NHL), significant proportions of patients relapse with incurable disease. The effect of human bone marrow (BM) mesenchymal stem cells (MSC) on tumor cell growth is controversial, and no specific information is available on the effect of BM-MSC on NHL. Methodology/Principal Findings The effect of BM-MSC was analyzed in two in vivo models of disseminated non-Hodgkin's lymphomas with an indolent (EBV− Burkitt-type BJAB, median survival = 46 days) and an aggressive (EBV+ B lymphoblastoid SKW6.4, median survival = 27 days) behavior in nude-SCID mice. Intra-peritoneal (i.p.) i…

Pathologymedicine.medical_specialtyStromal cellTransplantation HeterologousMice Nudelcsh:Medicinemesenchimal stem cellsMice SCIDMiceimmune system diseaseshemic and lymphatic diseasesmesenchymal stem cells non-Hodgkin's lymphoma.AnimalsHumansMedicinehuman lymphoma xenograft; mesenchimal stem cellsOncology/Hematological Malignancieslcsh:ScienceSCID MiceMultidisciplinaryHematology/Bone Marrow and Stem Cell Transplantationbusiness.industryLymphoma Non-HodgkinLymphoblastlcsh:RMesenchymal stem cellNon-Hodgkin's LymphomaMesenchymal Stem CellsHematopoietic Stem Cellsmedicine.diseaseCoculture TechniquesLymphomaNon-Hodgkin's lymphomaEndothelial stem cellTransplantationApoptosislcsh:QHematology/Lymphomas and Chronic Lymphoblastic LeukemiabusinessMesenchymal Stem Cells; SCID Mice; Non-Hodgkin's LymphomaResearch Articlehuman lymphoma xenograft
researchProduct

Models of Biobanking and Tissue Preservation: RNA Quality in Archival Samples in Pathology Laboratories and “In Vivo Biobanking” by Tumor Xenografts …

2011

Tissue banks represent essential resources and platforms for biomedical research serving basic, translational, and clinical research projects. In this article, we describe 2 models of biobanking and tissue preservation with different approaches and aims. Archive tissue biobanking is described here as a resource of residual pathology tissues for translational research, which represents the huge clinical heterogeneity. In this context, managing of tissues and RNA quality in archive tissue are discussed. The other model of tissue biobanking is referred to as xenograft tissue banking, which represents an alternative method for obtaining large amounts of tissue, over an indefinite period, in so …

Pathologymedicine.medical_specialtyTissue PreservationMedicine (miscellaneous)RNAContext (language use)Translational researchCell BiologyGeneral MedicineBiologymedicine.diseaseBiobankGeneral Biochemistry Genetics and Molecular BiologybiobankingxenograftsIn vivoArchive Tissues; RNA; biobanking; xenografts; TMA (tissue microarrays)Tissue bankmedicineArchive TissuesArchive TissueRNASarcomaxenograftTMA (tissue microarrays)
researchProduct

Blood absorption capacity of different xenograft bone substitutes. An in-vitro study

2019

Background Commercially available xenograft blocks, claim to have adequate characteristics to interact with biological media and thus permitting biological fluid absorption. The objective of this in vitro study was to compare the blood absorption capacity of four different xenograft block materials of different composition of collagen and porosity. Material and Methods Four brands of xenograft block materials were used (NuOss®, Bio-Oss®, Osteobiol® and Smartbone®). Five samples of each brand were analyzed, making a total of 20 tests. Human blood was used as the absorption liquid for the present experiment. The time period, in which the block remains in contact with the blood, was registered…

Porosidad616.3Absorption (skin)Regeneració òssiaOsteoconductionBiological fluidOsteoconducción03 medical and health sciences0302 clinical medicineAbsorción de sangreBiomaterials and Bioengineering in DentistryXenoinjertoIn vitro studyXenoinjertsRegeneración óseaBone regenerationGeneral DentistryCol·lagenXenograftsPorositatChemistryResearchSignificant differenceBiomaterialSmall sample030206 dentistry:CIENCIAS MÉDICAS [UNESCO]Bone regeneration030220 oncology & carcinogenesisUNESCO::CIENCIAS MÉDICASAbsorption capacityOsteoconduccióColágenoCollagenPorosityBiomedical engineeringAbsorció de sangBlood absorption
researchProduct

Combined inhibition of Bcl-2 and NFκB synergistically induces cell death in cutaneous T-cell lymphoma.

2019

Abstract Therapeutic options for cutaneous T-cell lymphoma (CTCL) are limited and curative treatment regimens are not available. Thus, new targeted and well-tolerated therapeutic approaches are urgently needed. In this respect, we have recently shown that dimethyl fumerate (DMF) inhibits NF-κB acting as a survival factor in CTCL. Similarly, inhibition of the antiapoptotic protein B-cell lymphoma 2 (Bcl-2) has been shown to induce cell death in CTCL especially when combined with histone deacetylase inhibitors. Therefore, we hypothesized that inhibition of Bcl-2 should potentiate NF-κB inhibition in a novel combination treatment of CTCL. We show that, in vitro, the Bcl-2 inhibitors ABT-199 an…

Programmed cell deathT cellImmunologyAntineoplastic AgentsApoptosisBiochemistryMicehemic and lymphatic diseasesCell Line TumormedicineAnimalsHumansRNA Small InterferingCell ProliferationNeoplasm StagingCell DeathDose-Response Relationship Drugbusiness.industryCutaneous T-cell lymphomaNF-kappa BDrug SynergismCell BiologyHematologymedicine.diseaseXenograft Model Antitumor AssaysLymphomaLymphoma T-Cell CutaneousHistone Deacetylase InhibitorsDisease Models Animalmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureCancer researchRNA InterferenceHistone deacetylaseSignal transductionbusinessProtein BindingBlood
researchProduct

Integrative genomic and proteomic analyses identify targets for Lkb1 deficient metastatic lung tumors

2010

SummaryIn mice, Lkb1 deletion and activation of KrasG12D results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these primary and metastatic de novo lung cancers with integrated genomic and proteomic profiles, and have identified gene and phosphoprotein signatures associated with Lkb1 loss and progression to invasive and metastatic lung tumors. These studies revealed that SRC is activated in Lkb1-deficient primary and metastatic lung tumors, and that the combined inhibition of SRC, PI3K, and MEK1/2 resulted in synergistic tumor regression. These studies demonstrate that integrated genomic and proteomic analyses can be used to identify signaling pathw…

ProteomicsCancer ResearchLung NeoplasmsMAP Kinase Kinase 2MAP Kinase Kinase 1CELLCYCLEAMP-Activated Protein Kinasesmedicine.disease_causeMice0302 clinical medicineAMP-Activated Protein Kinase KinasesCell MovementCarcinoma Non-Small-Cell LungEnzyme InhibitorsNeoplasm MetastasisPhosphorylationLymph nodePhosphoinositide-3 Kinase Inhibitors0303 health sciencesTOR Serine-Threonine KinasesIntracellular Signaling Peptides and ProteinsGenomicsCell cycleProtein-Tyrosine KinasesPenetrance3. Good healthUp-RegulationGene Expression Regulation Neoplasticmedicine.anatomical_structuresrc-Family KinasesOncologySIGNALING030220 oncology & carcinogenesisDrug Therapy CombinationFemaleRNA InterferenceKRASSignal TransductionMice NudeBiologyProtein Serine-Threonine KinasesArticleProto-Oncogene Proteins p21(ras)03 medical and health sciencesCell Line TumorProto-Oncogene ProteinsmedicineCell AdhesionAnimalsHumansEpithelial–mesenchymal transitionProtein Kinase Inhibitors030304 developmental biologyFocal AdhesionsGene Expression ProfilingCell BiologyXenograft Model Antitumor AssaysMice Mutant StrainsGene expression profilingFocal Adhesion Protein-Tyrosine KinasesCancer cellCell TransdifferentiationCancer researchras ProteinsCarcinogenesis
researchProduct

ErbB-3 activation by NRG-1β sustains growth and promotes vemurafenib resistance in BRAF-V600E colon cancer stem cells (CSCs)

2015

Approximately 5-10% of metastatic colorectal cancers harbor a BRAF-V600E mutation, which is correlated with resistance to EGFR-targeted therapies and worse clinical outcome. Vice versa, targeted inhibition of BRAF-V600E with the selective inhibitor PLX 4032 (Vemurafenib) is severely limited due to feedback re-activation of EGFR in these tumors. Mounting evidence indicates that upregulation of the ErbB-3 signaling axis may occur in response to several targeted therapeutics, including Vemurafenib, and NRG-1β-dependent re-activation of the PI3K/AKT survival pathway has been associated with therapy resistance. Here we show that colon CSCs express, next to EGFR and ErbB-2, also significant amoun…

Proto-Oncogene Proteins B-rafMAPK/ERK pathwayIndolesReceptor ErbB-3Colorectal cancerNeuregulin-1colon cancer stem cellsMice NudeAntineoplastic AgentsMiceErbBErbB-3medicineAnimalsHumansNeuregulin 1VemurafenibClonogenic assayskin and connective tissue diseasesProtein kinase BneoplasmsPI3K/AKT/mTOR pathwayCell ProliferationOligonucleotide Array Sequence AnalysisNRG-1βSulfonamidesbiologyReverse Transcriptase Polymerase Chain Reactionbusiness.industryFlow Cytometrymedicine.diseaseImmunohistochemistryXenograft Model Antitumor AssaysVemurafenibOncologyDrug Resistance NeoplasmColonic NeoplasmsImmunologyNeoplastic Stem CellsCancer researchbiology.proteinbusinessPriority Research Papermedicine.drug
researchProduct