Search results for "Kemi"

showing 10 items of 2204 documents

Myeloid leukemia with transdifferentiation plasticity developing from T-cell progenitors

2016

Unfavorable patient survival coincides with lineage plasticity observed in human acute leukemias. These cases are assumed to arise from hematopoietic stem cells, which have stable multipotent differentiation potential. However, here we report that plasticity in leukemia can result from instable lineage identity states inherited from differentiating progenitor cells. Using mice with enhanced c-Myc expression, we show, at the single-cell level, that T-lymphoid progenitors retain broad malignant lineage potential with a high capacity to differentiate into myeloid leukemia. These T-cell-derived myeloid blasts retain expression of a defined set of T-cell transcription factors, creating a lymphoi…

0301 basic medicineMyeloidBone Marrow CellsBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceshemic and lymphatic diseasesmedicineCell LineageProgenitor cellMolecular BiologyGeneral Immunology and MicrobiologyGeneral NeuroscienceTransdifferentiationMyeloid leukemiaCell DifferentiationArticlesmedicine.diseaseHematopoietic Stem CellsHaematopoiesisLeukemia030104 developmental biologymedicine.anatomical_structureImmunologyCancer researchLymphoid Progenitor CellsStem cell
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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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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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PTTG1-interacting protein (PTTG1IP/PBF) predicts breast cancer survival.

2017

Background: PTTG1-interacting protein (PTTG1IP) is an oncogenic protein, which participates in metaphase-anaphase transition of the cell cycle through activation of securin (PTTG1). PTTG1IP promotes the shift of securin from the cell cytoplasm to the nucleus, allowing the interaction between separase and securin. PTTG1IP overexpression has been previously observed in malignant disease, e.g. in breast carcinoma. However, the prognostic value of PTTG1IP in breast carcinoma patients has not previously been revealed. Methods: A total of 497 breast carcinoma patients with up to 22-year follow-up were analysed for PTTG1IP and securin immunoexpression. The results were evaluated for correlations w…

0301 basic medicineOncologyCancer ResearchTriple Negative Breast NeoplasmsKaplan-Meier EstimatePBF0302 clinical medicineBreast cancerSurgical oncologyRisk FactorsAged 80 and overrintasyöpäPTTG1 interacting proteinIntracellular Signaling Peptides and ProteinsCell cycleMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisImmunohistochemistrySecurinsyöpägeenitOncologySecurin030220 oncology & carcinogenesisImmunohistochemistryFemaleSeparaseBreast carcinomaResearch ArticleAdultmedicine.medical_specialtyPTTG1IPBreast Neoplasmslcsh:RC254-282immunohistokemia03 medical and health sciencesBreast cancerInternal medicineGeneticsmedicineBiomarkers TumorHumansAgedbusiness.industryMembrane Proteinsmedicine.disease030104 developmental biologyMultivariate AnalysisCancer researchprognosisproteiinitbusinessBMC cancer
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Genetically Determined Height and Risk of Non-hodgkin Lymphoma

2020

Although the evidence is not consistent, epidemiologic studies have suggested that taller adult height may be associated with an increased risk of some non-Hodgkin lymphoma (NHL) subtypes. Height is largely determined by genetic factors, but how these genetic factors may contribute to NHL risk is unknown. We investigated the relationship between genetic determinants of height and NHL risk using data from eight genome-wide association studies (GWAS) comprising 10,629 NHL cases, including 3,857 diffuse large B-cell lymphoma (DLBCL), 2,847 follicular lymphoma (FL), 3,100 chronic lymphocytic leukemia (CLL), and 825 marginal zone lymphoma (MZL) cases, and 9,505 controls of European ancestry. We …

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyChronic lymphocytic leukemiaFollicular lymphomadiffuse large B-cell lymphomaSingle-nucleotide polymorphismGenome-wide association studylcsh:RC254-28203 medical and health sciences0302 clinical medicinefollicular lymphomaimmune system diseasesInternal medicinehemic and lymphatic diseasesGeneticsMedicineLeucèmia limfocítica crònicageneticsOriginal ResearchGenetic associationCancer och onkologibusiness.industrynon-Hodgkin lymphomaOdds ratiomedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmarginal zone lymphomaLymphomaMalaltia de Hodgkin030104 developmental biologyOncologyCancer and Oncology030220 oncology & carcinogenesispolygenic risk scorediffuse large B-celllymphomachronic lymphocytic leukemiaChronic lymphocytic leukemiaHodgkin's diseasegeneticbusinessDiffuse large B-cell lymphomaGenèticaheightFrontiers in Oncology
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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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Focal Adhesion Genes Refine the Intermediate-Risk Cytogenetic Classification of Acute Myeloid Leukemia

2018

© 2018 by the authors.

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyNPM1PTK2acute myeloid leukemialcsh:RC254-282Article03 medical and health sciences0302 clinical medicinePTK2BLYNInternal medicinehemic and lymphatic diseasesmedicineLYNprognostic factorPrognostic factorintermediate-riskPTK2BAcute myeloid leukemiaPTK2business.industryMyeloid leukemialcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologyOncology030220 oncology & carcinogenesisCohortIntermediate-riskbusinessTyrosine kinaseProto-oncogene tyrosine-protein kinase SrcCancers
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High BCR-ABL/GUS(IS) levels at diagnosis of chronic phase CML are associated with unfavorable responses to standard-dose imatinib

2017

Abstract Purpose: The approval of second-generation tyrosine kinase inhibitors (TKIs) for the first-line treatment of chronic myeloid leukemia (CML) has generated an unmet need for baseline molecular parameters associated with inadequate imatinib responses. Experimental Design: We correlated BCR–ABL/GUSIS and BCR–ABL/ABL transcripts at diagnosis with the outcome—defined by the 2013 European LeukemiaNet recommendations—of 272 patients newly diagnosed with CML receiving imatinib 400 mg/daily. Applying receiver-operating characteristic curves, we defined BCR–ABL/GUSIS and BCR–ABL/ABL levels associated with lower probabilities of optimal response, failure-free (FFS), event-free (EFS), transform…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyPathologyMyeloidBCR-ABL Diagnosis CMLDrug intolerance03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesInternal medicineDiagnosismedicineBCR-ABLCMLneoplasmsABLbusiness.industryCancerMyeloid leukemiaImatinibOncology cancer researchmedicine.diseaseLeukemia030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisbusinessTyrosine kinasemedicine.drug
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Intermittent targeted therapies and stochastic evolution in patients affected by chronic myeloid leukemia

2016

Front line therapy for the treatment of patients affected by chronic myeloid leukemia (CML) is based on the administration of tyrosine kinase inhibitors, namely imatinib or, more recently, axitinib. Although imatinib is highly effective and represents an example of a successful molecular targeted therapy, the appearance of resistance is observed in a proportion of patients, especially those in advanced stages. In this work, we investigate the appearance of resistance in patients affected by CML, by modeling the evolutionary dynamics of cancerous cell populations in a simulated patient treated by an intermittent targeted therapy. We simulate, with the Monte Carlo method, the stochastic evolu…

0301 basic medicineOncologyDrugStatistics and Probabilitymedicine.medical_specialtymedicine.medical_treatmentmedia_common.quotation_subjectTargeted therapy03 medical and health sciencesClassical Monte Carlo simulations; computational biology; models for evolution (theory); mutational and evolutionary processes (theory); Statistical and Nonlinear Physics; Statistics and Probability; Statistics Probability and Uncertainty0302 clinical medicinecomputational biologyInternal medicinemedicineClassical Monte Carlo simulationmutational and evolutionary processes (theory)media_commonbusiness.industryMyeloid leukemiaStatistical and Nonlinear PhysicsImatinibSettore FIS/07 - Fisica Applicata(Beni Culturali Ambientali Biol.e Medicin)Axitinib030104 developmental biology030220 oncology & carcinogenesisCancer cellToxicityStatistics Probability and Uncertaintybusinessmodels for evolution (theory)Tyrosine kinasemedicine.drugStatistical and Nonlinear Physic
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