Search results for "Stem Cell"

showing 10 items of 2354 documents

PO-162 Long non coding RNA H19 (IncH19) is required for the hypoxia mediated multiple myeloma progression

2018

ABSTRACT Introduction Multiple myeloma (MM) is a malignant disorder of post-germinal centre B cells, characterised by the clonal proliferation of malignant plasma cells within the bone marrow (BM). The hypoxic condition that develops in the BM niche during progression of MM, has been shown to play a major role in i) the dissemination of MM, ii) the proliferation of MM cells and iii) the induction of drug resistance finally determining a poor prognosis for MM patients. The molecular mechanisms driving hypoxic responses is the activation and nuclear translocation of the Hypoxia-inducible factor 1-alpha, (HIF1α) that, in turns, induce the expression of genes controlling angiogenesis, hypermeta…

Cancer ResearchChemistryAngiogenesisMesenchymal stem cellStimulationHypoxia (medical)medicine.anatomical_structureHIF1AOncologyCell culturemedicineCancer researchGene silencingBone marrowmedicine.symptomESMO Open
researchProduct

PO-146 Multiple myeloma-derived exosomes carry amphiregulin and are responsible for the uncoupled bone remodelling

2018

Introduction Multiple myeloma (MM) is a hematologic malignancy associated with osteolytic bone disease caused by the perturbation of the functional balance between bone resorption and bone formation. Exosomes, nanosize lipoproteic structures, have been recently recognised as a new mechanism of cell to cell communication during tumour growth and progression. We have previously shown that MM-exosomes are involved in osteolytic lesions but the underlying mechanism is still understood. We hypothesise that the epidermal growth factor receptor ligand Amphiregulin (AREG) can be delivered by multiple myeloma-derived exosomes and participate in modulating the response of the bone microenvironment to…

Cancer ResearchChemistryMesenchymal stem cellExosomeBone resorptionMicrovesiclesBone remodelingmedicine.anatomical_structureOncologyAmphiregulinCell cultureOsteoclastmedicineCancer researchESMO Open
researchProduct

IL1β Induces Mesenchymal Stem Cells Migration and Leucocyte Chemotaxis Through NF-κB

2012

Mesenchymal stem cells are often transplanted into inflammatory environments where they are able to survive and modulate host immune responses through a poorly understood mechanism. In this paper we analyzed the responses of MSC to IL-1β: a representative inflammatory mediator. Microarray analysis of MSC treated with IL-1β revealed that this cytokine activateds a set of genes related to biological processes such as cell survival, cell migration, cell adhesion, chemokine production, induction of angiogenesis and modulation of the immune response. Further more detailed analysis by real-time PCR and functional assays revealed that IL-1β mainly increaseds the production of chemokines such as CC…

Cancer ResearchChemokineMigration and adhesionmedicine.medical_treatmentInterleukin-1betaBiologyArticleInterleukin 1βExtracellular matrixCell MovementCell AdhesionLeukocytesmedicineHumansCell adhesionCell ProliferationOligonucleotide Array Sequence AnalysisCell adhesion moleculeGene Expression ProfilingChemotaxisNF-kappa BMesenchymal Stem CellsCell migrationCell BiologyFibronectinsI-kappa B KinaseCell biologyChemotaxis LeukocyteHEK293 CellsCXCL3CytokineGene Knockdown Techniquesbiology.proteinIntercellular Signaling Peptides and ProteinsRNA InterferenceCollagenLamininChemokinesInflammation MediatorsStem cellSignal TransductionDevelopmental BiologyStem Cell Reviews and Reports
researchProduct

Response to imatinib in patients who relapse after allogeneic stem cell transplantation for chronic myeloid leukemia

2003

We studied 128 patients with chronic myeloid leukemia (CML) relapsing after allogeneic stem cell transplantation (SCT). Disease at the time of treatment with Imatinib was in chronic phase (CP) in 51 patients, accelerated phase (AP) in 31 and blastic crisis (BC) in 46. Of the 51 patients in CP, 14 were in cytogenetic and two in molecular relapses. The median interval between relapse and Imatinib therapy was 5 months (0–65). A total of 50 patients had failed treatment with donor lymphocyte infusions prior to Imatinib. The overall hemato-logical response rate was 84% (98% for patients relapsing in CP). The complete cytogenetic response (CCR) was 58% for patients in CP, 48% for AP and 22% for p…

Cancer ResearchChemotherapymedicine.medical_specialtybusiness.industrymedicine.medical_treatmentLymphocyteMyeloid leukemiaImatinibHematologyGastroenterologyTransplantationmedicine.anatomical_structureOncologyhemic and lymphatic diseasesInternal medicineImmunologymedicineIn patientStem cellbusinessAccelerated phasemedicine.drugLeukemia
researchProduct

STAT5 and STAT5 Inhibitors in Hematological Malignancies

2019

The JAK-STAT pathway is an important physiologic regulator of different cellular functions including proliferation, apoptosis, differentiation, and immunological responses. Out of six different STAT proteins, STAT5 plays its main role in hematopoiesis and constitutive STAT5 activation seems to be a key event in the pathogenesis of several hematological malignancies. This has led many researchers to develop compounds capable of inhibiting STAT5 activation or interfering with its functions. Several anti-STAT5 molecules have shown potent STAT5 inhibitory activity in vitro. However, compared to the large amount of clinical studies with JAK inhibitors that are currently widely used in the clini…

Cancer ResearchFLT3-ITDAntineoplastic Agents03 medical and health sciences0302 clinical medicineMyeloproliferative DisordersCancer stem cellSettore BIO/13 - Biologia Applicatahemic and lymphatic diseasesSTAT5 Transcription FactormedicineAnimalsHumansBCR-ABLSTAT5030304 developmental biologyPharmacology0303 health sciencesSTAT transcription factorbiologybusiness.industryfood and beveragesCancerHematopoietic stem cellMyeloid leukemiamedicine.diseaseSTAT5 inhibitorleukemia.Leukemiamedicine.anatomical_structureHematologic Neoplasms030220 oncology & carcinogenesisJak2V617Fbiology.proteinCancer researchSettore BIO/14 - FarmacologiaMolecular MedicinebusinessTyrosine kinase
researchProduct

Transcriptomic responses generated by hepatocarcinogens in a battery of liver-based in vitro models

2013

As the conventional approach to assess the potential of a chemical to cause cancer in humans still includes the 2-year rodent carcinogenicity bioassay, development of alternative methodologies is needed. In the present study, the transcriptomics responses following exposure to genotoxic (GTX) and non-genotoxic (NGTX) hepatocarcinogens and non-carcinogens (NC) in five liver-based in vitro models, namely conventional and epigenetically stabilized cultures of primary rat hepatocytes, the human hepatoma-derived cell lines HepaRG and HepG2 and human embryonic stem cell-derived hepatocyte-like cells, are examined. For full characterization of the systems, several bioinformatics approaches are emp…

Cancer ResearchGene Expressiongene expression profilingComputational biologyBiologyPharmacologyTranscriptomeRats Sprague-Dawley03 medical and health sciences0302 clinical medicineCell Line TumorBioassayAnimalsHumansGeneCarcinogenEmbryonic Stem Cells030304 developmental biology0303 health sciencesGene Expression ProfilingLiver Neoplasmspathwaysbased analysis liver-based in vitro modelGeneral MedicineHep G2 CellsEmbryonic stem cellIn vitro3. Good healthRatsgenotoxic carcinogens non-genotoxic carcinogensGene expression profilingLiverCell culture030220 oncology & carcinogenesisCarcinogensHepatocytesTumor Suppressor Protein p53TranscriptomeMutagens
researchProduct

Cancer stem cell definitions and terminology:the devil is in the details

2012

The cancer stem cell (CSC) concept has important therapeutic implications, but its investigation has been hampered both by a lack of consistency in the terms used for these cells and by how they are defined. Evidence of their heterogeneous origins, frequencies and their genomic, as well as their phenotypic and functional, properties has added to the confusion and has fuelled new ideas and controversies. Participants in The Year 2011 Working Conference on CSCs met to review these issues and to propose a conceptual and practical framework for CSC terminology. More precise reporting of the parameters that are used to identify CSCs and to attribute responses to them is also recommended as key t…

Cancer ResearchGeneral MathematicsACUTE MYELOID-LEUKEMIAPERIPHERAL-BLOODBiologyAnimals; Cell Differentiation; Cell Transformation Neoplastic; Clonal Evolution; Humans; Neoplastic Stem Cells; Terminology as Topic; Oncology; Cancer ResearchBioinformaticsCell TransformationSomatic evolution in cancerTumor Initiating CellsTerminologyClonal EvolutionIN-VITRO PROPAGATIONPHENOTYPIC HETEROGENEITYREPOPULATING CELLSConsistency (negotiation)Cancer stem cellCancer stem cells (CSC)Settore MED/04 - PATOLOGIA GENERALETerminology as TopicmedicineAnimalsHumansIn patientACUTE LYMPHOBLASTIC-LEUKEMIAGENE-EXPRESSIONConfusionSettore MED/04 - Patologia GeneraleMELANOMA-CELLSCognitive scienceNeoplasticAnimalApplied MathematicsSTEM/PROGENITOR CELLSCell DifferentiationTUMOR-INITIATING CELLSPeripheral bloodCell Transformation Neoplasticcancer stem cells differentiation tumor definitionsOncologyNeoplastic Stem CellsNeoplastic Stem Cellmedicine.symptomHuman
researchProduct

Optimization of retroviral-mediated gene transfer to human NOD/SCID mouse repopulating cord blood cells through a systematic analysis of protocol var…

1999

Abstract Retroviral transduction of human hematopoietic stem cells is still limited by lack of information about conditions that will maximize stem cell self-renewal divisions in vitro. To address this, we first compared the kinetics of entry into division of single human CD34 + CD38 − cord blood (CB) cells exposed in vitro to three different flt3-ligand (FL)-containing cytokine combinations. Of the three combinations tested, FL + hyperinterleukin 6 (HIL-6) yielded the least clones and these developed at a slow rate. With either FL + Steel factor (SF) + HIL-6 + thrombopoietin (TPO) or FL + SF + interleukin 3 (IL-3) + IL-6 + granulocyte-colony-stimulating factor (G-CSF), >90% of the cells th…

Cancer ResearchGenetic VectorsCD34Antigens CD34Stem cell factorMice SCIDCD38BiologyImmunophenotypingViral vectorMiceNAD+ NucleosidaseAntigens CDMice Inbred NODTransduction GeneticGeneticsAnimalsHumansADP-ribosyl CyclaseMolecular BiologyInterleukin 3Membrane GlycoproteinsGene Transfer TechniquesInfant NewbornMembrane ProteinsCell BiologyHematologyFetal BloodADP-ribosyl Cyclase 1Antigens DifferentiationVirologyMolecular biologyHaematopoiesisRetroviridaeCord bloodStem cellCell DivisionExperimental Hematology
researchProduct

Aberrations of Genomic Imprinting in Glioblastoma Formation

2021

In human glioblastoma (GBM), the presence of a small population of cells with stem cell characteristics, the glioma stem cells (GSCs), has been described. These cells have GBM potential and are responsible for the origin of the tumors. However, whether GSCs originate from normal neural stem cells (NSCs) as a consequence of genetic and epigenetic changes and/or dedifferentiation from somatic cells remains to be investigated. Genomic imprinting is an epigenetic marking process that causes genes to be expressed depending on their parental origin. The dysregulation of the imprinting pattern or the loss of genomic imprinting (LOI) have been described in different tumors including GBM, being one …

Cancer ResearchGenomic imprintingSomatic cellSubventricular zonePopulationReviewBiologylcsh:RC254-282MethylationGliomamedicineEpigeneticsImprinting (psychology)educationneural stem cellsNeural stem cellseducation.field_of_studyglioblastomasubventricular zonelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseNeural stem cellgenomic imprintingnervous system diseasesOncologyCancer researchmethylationStem cellGenomic imprintingGlioblastoma
researchProduct

The AC133 epitope, but not the CD133 protein, is lost upon cancer stem cell differentiation.

2010

Abstract Colon cancer stem cells (CSC) can be identified with AC133, an antibody that detects an epitope on CD133. However, recent evidence suggests that expression of CD133 is not restricted to CSCs, but is also expressed on differentiated tumor cells. Intriguingly, we observed that detection of the AC133 epitope on the cell surface decreased upon differentiation of CSC in a manner that correlated with loss of clonogenicity. However, this event did not coincide with a change in CD133 promoter activity, mRNA, splice variant, protein expression, or even cell surface expression of CD133. In contrast, we noted that with CSC differentiation, a change occured in CD133 glycosylation. Thus, AC133 …

Cancer ResearchGlycosylationGlycosylationCellular differentiationCellAC 133 EpitopeDown-RegulationMice SCIDEpitopechemistry.chemical_compoundEpitopesMiceCancer stem cellAntigens CDMice Inbred NODProminin-1medicineTumor Cells CulturedAnimalsHumansProtein IsoformsAC133 AntigenRNA MessengerPromoter Regions GeneticneoplasmsGlycoproteinsbiologyCell DifferentiationMolecular biologycarbohydrates (lipids)Gene Expression Regulation Neoplasticmedicine.anatomical_structureOncologychemistryembryonic structuresColonic Neoplasmsbiology.proteinNeoplastic Stem CellsAntibodyStem cellPeptidesCancer research
researchProduct