Search results for "Myeloid"

showing 10 items of 538 documents

Bis(1H-indol-2-yl)methanones are effective inhibitors of FLT3-ITD tyrosine kinase and partially overcome resistance to PKC412A in vitro.

2009

Inhibition of the mutated fms-like tyrosine kinase 3 (FLT3) receptor tyrosine kinase is a promising therapeutic strategy in acute myeloid leukaemia (AML). However, development of resistance to FLT3 tyrosine kinase inhibitors (TKI), such as PKC412A, has been described recently. This observation may have an increasing impact on the duration of response and relapse rates in upcoming clinical trials employing FLT3-TKI. Herein we investigated two representatives of a novel class of FLT3-TKI: Bis(1H-indol-2-yl)methanones. Both compounds effectively induced apoptosis in FLT3-internal tandem duplicate (ITD)-transfected murine myeloid cells and in primary FLT3-ITD positive blasts. Combination of bot…

MAPK/ERK pathwayIndolesmedicine.drug_classAntineoplastic AgentsApoptosisTransfectionTyrosine-kinase inhibitorReceptor tyrosine kinaseCell Linefluids and secretionshemic and lymphatic diseasesmedicineTumor Cells CulturedHumansProtein kinase Bbiologyhemic and immune systemsHematologyStaurosporineIn vitroLeukemia Myeloid Acutefms-Like Tyrosine Kinase 3Drug Resistance NeoplasmTandem Repeat SequencesTrk receptorembryonic structuresFms-Like Tyrosine Kinase 3Cancer researchbiology.proteinTyrosine kinasepsychological phenomena and processesBritish journal of haematology
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Therapeutic resistance resulting from mutations in Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR signaling pathways.

2011

Chemotherapy remains a commonly used therapeutic approach for many cancers. Indeed chemotherapy is relatively effective for treatment of certain cancers and it may be the only therapy (besides radiotherapy) that is appropriate for certain cancers. However, a common problem with chemotherapy is the development of drug resistance. Many studies on the mechanisms of drug resistance concentrated on the expression of membrane transporters and how they could be aberrantly regulated in drug resistant cells. Attempts were made to isolate specific inhibitors which could be used to treat drug resistant patients. Unfortunately most of these drug transporter inhibitors have not proven effective for ther…

MAPK/ERK pathwayPTENTumor suppressor genekinase inhibitorPhysiologymedicine.medical_treatmentClinical Biochemistrygrowth factor receptorAntineoplastic AgentsDrug resistancePharmacologyBiologyTargeted therapy03 medical and health sciencesMicePhosphatidylinositol 3-Kinases0302 clinical medicineGrowth factor receptormedicinePTENAnimalsHumansExtracellular Signal-Regulated MAP KinasesProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesTOR Serine-Threonine KinasesPTEN PhosphohydrolaseCell BiologyMAP Kinase Kinase Kinases3. Good healthErbB ReceptorsDrug Resistance Neoplasm030220 oncology & carcinogenesisMutationCancer researchbiology.proteinraf KinasesProto-Oncogene Proteins c-aktDrug resistance therapeutic sensitivity targeted therapy RAF ERKACUTE MYELOID LEUKAEMIASignal TransductionJournal of cellular physiology
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Symplekin, a polyadenylation factor, prevents MOZ and MLL activity on HOXA9 in hematopoietic cells

2013

International audience; MOZ and MLL encoding a histone acetyltransferase and a histone methyltransferase, respectively, are targets for recurrent chromosomal translocations found in acute myeloblastic or lymphoblastic leukemia. We have previously shown that MOZ and MLL cooperate to activate HOXA9 gene expression in hematopoietic stem/progenitors cells. To dissect the mechanism of action of this complex, we decided to identify new proteins interacting with MOZ. We found that the scaffold protein Symplekin that supports the assembly of polyadenylation machinery was identified by mass spectrometry. Symplekin interacts and co-localizes with both MOZ and MLL in immature hematopoietic cells. Its …

MLLScaffold proteinPolyadenylationHematopoietic System[SDV]Life Sciences [q-bio]PolyadenylationCell Line03 medical and health scienceschemistry.chemical_compound0302 clinical medicinehemic and lymphatic diseasesGene expressionTranscriptional regulationHumansRNA MessengerPromoter Regions GeneticSymplekinHSF1neoplasmsMolecular BiologyHistone Acetyltransferases030304 developmental biologyHomeodomain ProteinsmRNA Cleavage and Polyadenylation Factors0303 health sciences[ SDV ] Life Sciences [q-bio]biologyNuclear ProteinsHistone-Lysine N-MethyltransferaseHOXA9Transcription regulationCell BiologyHistone acetyltransferaseMOZCell biology[SDV] Life Sciences [q-bio]Protein TransportRUNX1chemistry030220 oncology & carcinogenesisHistone methyltransferaseCancer researchbiology.proteinMyeloid-Lymphoid Leukemia ProteinProtein BindingBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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A newly established murine immature dendritic cell line can be differentiated into a mature state, but exerts tolerogenic function upon maturation in…

2007

AbstractThe phenotype and function of murine dendritic cells (DCs) are primarily studied using bone-marrow–derived DCs (BM-DCs), but may be hampered by the heterogenous phenotype of BM-DCs due to their differential state of maturation. Here we characterize a newly established murine DC line (SP37A3) of myeloid origin. During maintainance in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF) and M-CSF, SP37A3 cells resemble immature DCs characterized by low expression of major histocompatibility complex (MHC) II and costimulatory molecules and low T-cell stimulatory capacity. Upon stimulation, SP37A3 cells acquire a mature phenotype and activate naive T cells as potent…

Macrophage colony-stimulating factorMyeloidmedicine.medical_treatmentImmunologyBiologyMajor histocompatibility complexT-Lymphocytes RegulatoryBiochemistryDexamethasoneCell LineMicemedicineAnimalsGlucocorticoidsMyeloid Progenitor CellsCell ProliferationClonal AnergyMice Inbred BALB CFollicular dendritic cellsReceptors IgGHistocompatibility Antigens Class IICell DifferentiationDendritic CellsCell BiologyHematologyDendritic cellCoculture TechniquesUp-RegulationCell biologyInterleukin 1 Receptor Antagonist ProteinGranulocyte macrophage colony-stimulating factormedicine.anatomical_structureCytokineCell culturebiology.proteinCytokinesmedicine.drugBlood
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Essential Oil Composition of

2019

Drug resistance is a major obstacle in antibiotic and antitumor chemotherapy. In response to the necessity to find new therapeutic strategies, plant secondary metabolites including essential oils (EOs) may represent one of the best sources. EOs in plants act as constitutive defenses against biotic and abiotic stress, and they play an important role in the pharmacology for their low toxicity, good pharmacokinetic and multitarget activity. In this context, natural products such as EOs are one of the most important sources of drugs used in pharmaceutical therapeutics. The aim of this paper was to identify the chemical composition of the essential oil of Alluaudia procera leaves, obtained by hy…

MagnoliopsidaMolecular StructureSpectrum AnalysisPhytochemicalsDrug ResistanceOils VolatileAntineoplastic AgentsArticleessential oilacute myeloid leukemia cellAnti-Bacterial AgentsDidiereaceaesucculent plantsMolecules (Basel, Switzerland)
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Influence of cytarabine metabolic pathway polymorphisms in acute myeloid leukemia induction treatment

2017

Cytarabine is considered the most effective chemotherapeutic option in acute myeloid leukemia (AML). The impact of 10 polymorphisms in cytarabine metabolic pathway genes were evaluated in 225 adult de novo AML patients. Variant alleles of DCK rs2306744 and CDA rs602950 showed higher complete remission (p = .024, p = .045), with lower survival rates for variant alleles of CDA rs2072671 (p = .015, p = .045, p = .032), rs3215400 (p = .033) and wild-type genotype of rs602950 (p = .039, .014). Induction death (p = .033) and lower survival rates (p = .021, p = .047) were correlated to RRM1 rs9937 variant allele. In addition, variant alleles of CDA rs532545 and rs602950 were related to skin toxici…

Male0301 basic medicineOncologyCancer ResearchPharmacogenomic VariantsefficacyKaplan-Meier Estimatepolymorphism0302 clinical medicinePolymorphism (computer science)GenotypeRemission InductionCytarabineDCKMyeloid leukemiaHematologyMiddle AgedPrognosisLeukemia Myeloid AcuteOncology030220 oncology & carcinogenesisToxicityFemaleMetabolic Networks and Pathwaysmedicine.drugAdultAntimetabolites Antineoplasticmedicine.medical_specialtyAdolescentGenotypeacute myeloid leukemiaPolymorphism Single NucleotideYoung Adult03 medical and health sciencesInternal medicinemedicineMucositisHumansAlleleAllelesAgedRetrospective StudiesPolymorphism Geneticbusiness.industrymedicine.diseaseMinor allele frequency030104 developmental biologyCDAImmunologyCytarabinebusiness
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Impact ofABCsingle nucleotide polymorphisms upon the efficacy and toxicity of induction chemotherapy in acute myeloid leukemia

2016

Anthracycline uptake could be affected by efflux pumps of the ABC family. The influence of 7 SNPs of ABC genes was evaluated in 225 adult de novo acute myeloid leukemia (AML) patients. After multivariate logistic regression there were no significant differences in complete remission, though induction death was associated to ABCB1 triple variant haplotype (p = .020). The ABCB1 triple variant haplotype was related to higher nephrotoxicity (p = .016), as well as this haplotype and the variant allele of ABCB1 rs1128503, rs2032582 to hepatotoxicity (p = .001; p = .049; p  .001). Furthermore, the variant allele of ABCC1 rs4148350 was related to severe hepatotoxicity (p = .044), and the variant al…

Male0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyGenotypePharmacogenomic Variantsmedicine.medical_treatmentSingle-nucleotide polymorphismNeutropeniaBiologyPolymorphism Single Nucleotide03 medical and health sciences0302 clinical medicineInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansIdarubicinProspective cohort studyAllelesAgedRetrospective StudiesAged 80 and overChemotherapyHaplotypeInduction chemotherapyMyeloid leukemiaInduction ChemotherapyHematologyMiddle Agedmedicine.diseaseLeukemia Myeloid AcuteTreatment Outcome030104 developmental biologyAmino Acid SubstitutionOncology030220 oncology & carcinogenesisImmunologyATP-Binding Cassette TransportersFemaleBiomarkersmedicine.drugLeukemia & Lymphoma
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Clinical Implications of Discordant Early Molecular Responses in CML Patients Treated with Imatinib

2019

A reduction in BCR-ABL1/ABL1IS transcript levels to &lt

Male0301 basic medicineOncologyTreatment outcomeFusion Proteins bcr-ablAntineoplastic Agentlcsh:ChemistryBcr abl10302 clinical medicinehemic and lymphatic diseasesimatinib mesylateBCR-ABL1; European Leukemia Net; chronic myeloid leukemia; early molecular response; imatinib mesylatelcsh:QH301-705.5<i>BCR-ABL1</i>SpectroscopyAged 80 and overGeneral MedicineMiddle AgedComputer Science ApplicationsTreatment Outcome030220 oncology & carcinogenesisFemaleHumanmedicine.drugAdultmedicine.medical_specialtyProtein Kinase InhibitorAntineoplastic AgentsArticleCatalysisEuropean Leukemia NetInorganic Chemistry03 medical and health scienceschronic myeloid leukemiaLeukemia Myelogenous Chronic BCR-ABL PositiveInternal medicineBiomarkers TumormedicineHumansIn patientRNA MessengerPhysical and Theoretical ChemistryProtein Kinase InhibitorsMolecular BiologyAgedbusiness.industryOrganic ChemistryImatinibBCR-ABL1030104 developmental biologyImatinib mesylatelcsh:Biology (General)lcsh:QD1-999early molecular responsebusiness
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CpG islands in MyD88 and ASC/PYCARD/TMS1 promoter regions are differentially methylated in head and neck squamous cell carcinoma and primary lung squ…

2021

Abstract Background Patients with head and neck squamous cell carcinoma (HNSCC) can develop lung squamous cell carcinoma (LuSCC), which could be the second primary tumor or HNSCC metastasis. Morphologically it is difficult to distinguish metastatic HNSCC from a second primary tumor which presents a significant diagnostic challenge. Differentiation of those two malignancies is important because the recommended treatments for metastatic HNSCC and primary LuSCC differ significantly. We investigated if the quantification of the promotor methylation status in HNSCC and LuSCC differs. Methods Primary HNSCC (N = 36) and LuSCC (N = 17) were included in this study. Methylation status in the ASC/TMS1…

Male0301 basic medicinePathologyLung NeoplasmsHNSCCEpigenesis GeneticMetastasis0302 clinical medicinePromoter Regions GeneticLungDiagnostic biomarkerPYCARDGeneral MedicineMethylationMiddle AgedGene Expression Regulation NeoplasticBisulfiteCpG siteHead and Neck Neoplasms030220 oncology & carcinogenesisCarcinoma Squamous CellSecond primary tumorFemalelcsh:RB1-214Adultmedicine.medical_specialtyHistologyShort ReportBiologyMethylationPathology and Forensic Medicine03 medical and health sciencesCpG ; diagnostic biomarker ; HNSCC ; lung ; methylation ; second primary tumorCpGClinical Medical Scienceslcsh:PathologymedicineHumansGeneAdaptor Proteins Signal TransducingAgedSquamous Cell Carcinoma of Head and NeckPromotermedicine.diseaseHead and neck squamous-cell carcinomastomatognathic diseases030104 developmental biologyMyeloid Differentiation Factor 88Cancer researchCpG IslandsDiagnostic Pathology
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Prognostic value of FLT3 mutations in patients with acute promyelocytic leukemia treated with all-trans retinoic acid and anthracycline monochemother…

2011

Background Fms-like tyrosine kinase-3 (FLT3) gene mutations are frequent in acute promyelocytic leukemia but their prognostic value is not well established. Design and Methods We evaluated FLT3-internal tandem duplication and FLT3-D835 mutations in patients treated with all-trans retinoic acid and anthracycline-based chemotherapy enrolled in two subsequent trials of the Programa de Estudio y Tratamiento de las Hemopatias Malignas (PETHEMA) and Hemato-Oncologie voor Volwassenen Nederland (HOVON) groups between 1996 and 2005. Results FLT3-internal tandem duplication and FLT3-D835 mutation status was available for 306 (41%) and 213 (29%) patients, respectively. Sixty-eight (22%) and 20 (9%) pa…

MaleAIDA PROTOCOLGene mutationmedicine.disease_causeGastroenterologyLeukemia Promyelocytic AcuteRESIDUAL DISEASEhemic and lymphatic diseasesMOLECULAR SUBTYPESChildanthracyclinesMutationRemission InductionFLT3 mutationshemic and immune systemsHematologyMiddle AgedPrognosisall-trans retinoic acidLeukemiaTreatment Outcomeembryonic structuresFemaleTandem exon duplicationmedicine.drugAcute promyelocytic leukemiaAdultmedicine.medical_specialtyAdolescentAntineoplastic AgentsTretinoinACUTE MYELOID-LEUKEMIABiologyYoung AdultQUALITY-CONTROLTretinoinPOOR-PROGNOSISInternal medicinemedicineCoagulopathyHumansAgedprognostic factorsOriginal Articlesacute promyelocytic leukemiamedicine.diseaseSurvival AnalysisINTERNAL TANDEM DUPLICATIONRISK-ADAPTED TREATMENTPML/RAR-ALPHAfms-Like Tyrosine Kinase 3Fms-Like Tyrosine Kinase 3ImmunologyPETHEMA GROUPMutation
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