Search results for "Myeloid"

showing 10 items of 538 documents

Genome-wide miRNA profiling and pivotal roles of miRs 125a-5p and 17-92 cluster in human neutrophil maturation and differentiation of acute myeloid l…

2019

19 p.-7 fig.-1 tab.

0301 basic medicineMyeloidCellular differentiationCD34miR-125a-5pBiology03 medical and health sciences0302 clinical medicineNeutrophil differentiationDifferentiation therapyneutrophil differentiationmedicinehumanmiRNANeutrophil differentiationmiR-17-92Myeloid leukemiamedicine.diseaseCell biologyLeukemia030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisStem cellResearch PaperHumanOncotarget
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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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Myeloid cells as orchestrators of the tumor microenvironment: novel targets for nanoparticular cancer therapy.

2016

Macrophages, myeloid-derived suppressor cells and tolerogenic dendritic cells are central players of a heterogeneous myeloid cell population, with the ability to suppress innate and adaptive immune responses and thus to promote tumor growth. Their influx and local proliferation are mainly induced by the cancers themselves, and their numbers in the tumor microenvironment and the peripheral blood correlate with decreased survival. Therapeutic targeting these innate immune cells, either aiming at their elimination or polarization toward tumor suppressive cells is an attractive novel approach to control tumor progression and block metastasis. We review the current understanding of cancer immun…

0301 basic medicineMyeloidPolymersmedicine.medical_treatmentPopulationBiomedical EngineeringMedicine (miscellaneous)BioengineeringDevelopmentBiology03 medical and health sciences0302 clinical medicineImmune systemNeoplasmsmedicineTumor MicroenvironmentAnimalsHumansGeneral Materials ScienceMyeloid CellsRNA Small InterferingeducationCancer immunologyeducation.field_of_studyTumor microenvironmentDrug CarriersInnate immune systemMacrophagesMyeloid-Derived Suppressor CellsImmunotherapyDendritic CellsImmunity Innate030104 developmental biologymedicine.anatomical_structureTumor progression030220 oncology & carcinogenesisImmunologyNanoparticlesImmunotherapyNanomedicine (London, England)
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Myeloid cell-synthesized coagulation Factor X dampens anti-tumor immunity

2019

Immune evasion in the tumor microenvironment (TME) is a crucial barrier for effective cancer therapy, and plasticity of innate immune cells may contribute to failures of targeted immunotherapies. Here, we show that rivaroxaban, a direct inhibitor of activated coagulation factor X (FX), promotes antitumor immunity by enhancing infiltration of dendritic cells and cytotoxic T cells at the tumor site. Profiling FX expression in the TME identifies monocytes and macrophages as crucial sources of extravascular FX. By generating mice with immune cells lacking the ability to produce FX, we show that myeloid cell-derived FX plays a pivotal role in promoting tumor immune evasion. In mouse models of ca…

0301 basic medicineMyeloidmedicine.medical_treatmentImmunologyCellMammary Neoplasms AnimalArticle03 medical and health sciencesMice0302 clinical medicineImmune systemmedicineCytotoxic T cellAnimalsHumansMyeloid CellsTumor microenvironmentInnate immune systembusiness.industryGeneral MedicineImmunotherapyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisFactor XCancer researchFemaleImmunotherapySignal transductionbusiness
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Human leukocyte antigen-E mismatch is associated with better hematopoietic stem cell transplantation outcome in acute leukemia patients

2017

The immunomodulatory role of human leukocyte antigen (HLA)-E in hematopoietic stem cell transplantation (HSCT) has not been extensively investigated. To this end, we genotyped 509 10/10 HLA unrelated transplant pairs for HLA-E, in order to study the effect of HLA-E as a natural killer (NK)-alloreactivity mediator on HSCT outcome in an acute leukemia (AL) setting. Overall survival (OS), disease free survival (DFS), relapse incidence (RI) and non-relapse mortality (NRM) were set as endpoints. Analysis of our data revealed a significant correlation between HLA-E mismatch and improved HSCT outcome, as shown by both univariate (53% vs. 38%, P=0.002, 5-year OS) and multivariate (hazard ratio (HR)…

0301 basic medicineOncologyAdultMalemedicine.medical_specialtyTransplantation ConditioningAdolescentGenotypemedicine.medical_treatment610Hematopoietic stem cell transplantationHuman leukocyte antigen600 Technik Medizin angewandte Wissenschaften::610 Medizin und GesundheitArticle03 medical and health sciencesYoung Adult0302 clinical medicineCell Therapy & ImmunotherapyInternal medicineMedicineHumansTransplantation Homologousddc:610Potassium Channels Inwardly RectifyingSurvival analysisAllelesAgedBone Marrow TransplantationAcute leukemiabusiness.industryDonor selectionHistocompatibility TestingHazard ratioHistocompatibility Antigens Class IHematopoietic Stem Cell TransplantationHematologyMiddle Agedmedicine.diseasePrognosisSurvival AnalysisTransplantationLeukemiaLeukemia Myeloid Acute030104 developmental biologyTreatment OutcomeImmunologyFemalebusiness030215 immunology
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Impact of novel polymorphisms related to cytotoxicity of cytarabine in the induction treatment of acute myeloid leukemia.

2017

Several novel single nucleotide polymorphisms (SNPs) involved in cytarabine cytotoxicity and related to clinical outcomes have been reported recently in a series of 232 pediatric patients with acute myeloid leukemia (AML). We report the first adult AML cohort in which the influence of these SNPs in cytarabine efficacy and toxicity was analyzed. Six of polymorphisms with clinical significance in the previous study [rs12036333, rs10758713, rs9883101, rs6550826, IRX2: rs2897047, mutated in colorectal cancers (MCC): rs7729269] were analyzed in a cohort of 225 adult patients at initial diagnosis of AML treated with an induction scheme of idarubicin plus cytarabine. The variant alleles of rs12036…

0301 basic medicineOncologyAdultmedicine.medical_specialtyAdolescentPopulationSingle-nucleotide polymorphismKaplan-Meier EstimatePolymorphism Single NucleotideDisease-Free Survival03 medical and health sciencesYoung Adult0302 clinical medicineInternal medicineGeneticsmedicineIdarubicinHumansGeneral Pharmacology Toxicology and PharmaceuticseducationProspective cohort studyMolecular BiologyGenetics (clinical)Agededucation.field_of_studybusiness.industryCytarabineInduction chemotherapyMyeloid leukemiaInduction ChemotherapyMiddle AgedMinor allele frequencyLeukemia Myeloid Acute030104 developmental biology030220 oncology & carcinogenesisCytarabineMolecular Medicinebusinessmedicine.drugPharmacogenetics and genomics
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Accumulation of MDSC and Th17 Cells in Patients with Metastatic Colorectal Cancer Predicts the Efficacy of a FOLFOX-Bevacizumab Drug Treatment Regimen

2016

Abstract Host immunity controls the development of colorectal cancer, and chemotherapy used to treat colorectal cancer is likely to recruit the host immune system at some level. Athough preclinical studies have argued that colorectal cancer drugs, such as 5-fluorouracil (5-FU) and oxaliplatin, exert such effects, their combination as employed in the oncology clinic has not been evaluated. Here, we report the results of prospective immunomonitoring of 25 metastatic colorectal cancer (mCRC) patients treated with a first-line combination regimen of 5-FU, oxaliplatin, and bevacizumab (FOLFOX–bevacizumab), as compared with 20 healthy volunteers. Before this therapy was initiated, T regulatory ce…

0301 basic medicineOncologyCancer ResearchOrganoplatinum CompoundsColorectal cancermedicine.medical_treatmentLeucovorinKaplan-Meier EstimatePolymerase Chain ReactionSuppressor-Cells[ SDV.CAN ] Life Sciences [q-bio]/Cancer0302 clinical medicineFOLFOXAntineoplastic Combined Chemotherapy ProtocolsProspective StudiesProgressionFlow Cytometry3. Good healthBevacizumabOncology030220 oncology & carcinogenesisFluorouracilColorectal Neoplasmsmedicine.drugmedicine.medical_specialtyBevacizumabT-Cells[SDV.CAN]Life Sciences [q-bio]/CancerDisease-Free Survival03 medical and health sciencesInternal medicinemedicineCarcinomaHumansChemotherapyTumorsInflammationChemotherapyAntitumor Immunitybusiness.industryMyeloid-Derived Suppressor CellsCarcinomaCancermedicine.diseasedigestive system diseasesOxaliplatinRegimen030104 developmental biologyTherapiesImmunologyTh17 CellsPoor-Prognosisbusiness
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Baseline Splenic Volume as a Prognostic Biomarker of FOLFIRI Efficacy and a Surrogate Marker of MDSC Accumulation in Metastatic Colorectal Carcinoma

2020

Background: Predictive biomarkers of response to chemotherapy plus antiangiogenic for metastatic colorectal cancer (mCRC) are lacking. The objective of this study was to test the prognostic role of splenomegaly on baseline CT scan. Methods: This study is a sub-study of PRODIGE-9 study, which included 488 mCRC patients treated by 5-fluorouracil, leucovorin and irinotecan (FOLFIRI) and bevacizumab in first line. The association between splenic volume, and PFS and OS was evaluated by univariate and multivariable Cox analyses. The relation between circulating monocytic Myeloid derived suppressor cells (mMDSC) and splenomegaly was also determined. Results: Baseline splenic volume &gt

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyBevacizumabColorectal cancermedicine.medical_treatment[SDV]Life Sciences [q-bio]MDSClcsh:RC254-282Article03 medical and health sciences0302 clinical medicineInternal medicineMedicinePrognostic biomarkerprognostic biomarkerChemotherapysplenomegalybusiness.industrySurrogate endpointmetastatic colorectal cancerlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasedigestive system diseases3. Good healthIrinotecan030104 developmental biologyOncology030220 oncology & carcinogenesisMyeloid-derived Suppressor CellFOLFIRIcirculating monocytic myeloid derived suppressor cellsbusinessmedicine.drugCancers
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BCR-ABL1 Doubling-Times and Halving-Times May Predict CML Response to Tyrosine Kinase Inhibitors

2019

In Chronic Myeloid Leukemia (CML), successful treatment requires accurate molecular monitoring to evaluate disease response and provide timely interventions for patients failing to achieve the desired outcomes. We wanted to determine whether measuring BCR-ABL1 mRNA doubling-times (DTs) could distinguish inconsequential rises in the oncogene’s expression from resistance to tyrosine kinase inhibitors (TKIs). Thus, we retrospectively examined BCR-ABL1 evolution in 305 chronic-phase CML patients receiving imatinib mesylate (IM) as a first line treatment. Patients were subdivided in two groups: those with a confirmed rise in BCR-ABL1 transcripts without MR3.0 loss and those failing IM. We found …

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyDisease ResponseChronic Myeloid LeukemiaBCR-ABL1/ABL1IShalving-timelcsh:RC254-28203 medical and health sciences0302 clinical medicineInternal medicinehemic and lymphatic diseasesBCR-ABL1/ABL1; IS; Chronic Myeloid Leukemia; Doubling-time; Halving-time; Tyrosine kinase inhibitorstyrosine kinase inhibitorsmedicineDoubling timeOriginal ResearchBCR-ABL1/ABL1Oncogenebusiness.industryMyeloid leukemialcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensDiscontinuationdoubling-time030104 developmental biologyImatinib mesylateOncology030220 oncology & carcinogenesisCohortISBCR-ABL1/ABL1 ISbusinessTyrosine kinaseFrontiers in Oncology
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Evaluation of tumor immune contexture among intrinsic molecular subtypes helps to predict outcome in early breast cancer

2021

BackgroundThe prognosis of early breast cancer is linked to clinic-pathological stage and the molecular characteristics of intrinsic tumor cells. In some patients, the amount and quality of tumor-infiltrating immune cells appear to affect long term outcome. We aimed to propose a new tool to estimate immune infiltrate, and link these factors to patient prognosis according to breast cancer molecular subtypes.MethodsWe performed in silico analyses in more than 2800 early breast cancer transcriptomes with corresponding clinical annotations. We first developed a new gene expression deconvolution algorithm that accurately estimates the quantity of immune cell populations (tumor immune contexture,…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyMyeloid2435In silicoImmunologyCellbiostatisticsBreast NeoplasmsTranscriptome03 medical and health sciences0302 clinical medicineBreast cancerImmune systemLymphocytes Tumor-InfiltratingInternal medicinemedicineBiomarkers TumorImmunology and Allergytumor microenvironmentHumans1506Stage (cooking)RC254-282Neoplasm StagingPharmacologyClinical/Translational Cancer ImmunotherapyTumor microenvironmentbusiness.industryGene Expression ProfilingNeoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasePrognosisSurvival AnalysisGene Expression Regulation Neoplastic030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesistumor biomarkersMolecular MedicineFemalebusinessAlgorithmsUnsupervised Machine LearningJournal for Immunotherapy of Cancer
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