Search results for "leukemia"

showing 10 items of 976 documents

Histone deacetylase inhibition modulates deoxyribonucleotide pools and enhances the antitumor effects of the ribonucleotide reductase inhibitor 3’-C-…

2011

Histone deacetylase (HDAC) inhibitors are a new class of epigenetic agents that were reported to enhance the cytotoxic effects of classical anticancer drugs through multiple mechanisms. However, which of the possible drug combinations would be the most effective and clinically useful are to be determined. We treated the HL60 and NB4 promyelocytic leukaemia cells with a combination of the ribonucleotide reductase (RR) inhibitor 3'-C-methyladenosine (3'-Me-Ado) and several hydroxamic acid-derived HDAC inhibitors, including two recently synthesized molecules, MC1864 and MC1879, and the reference compound trichostatin A (TSA). The results showed significant growth inhibitory and apoptotic syner…

Cancer ResearchAdenosineHL60CellDeoxyribonucleotidesAntineoplastic AgentsApoptosisHL-60 CellsRibonucleotide reductase inhibitorBiologyHydroxamic AcidsHDAC inhibitors RR inhibitors Apoptosis Leukaemia ROSchemistry.chemical_compoundRibonucleotide ReductasesmedicineHumansCell ProliferationLeukemiaG1 PhaseCell cycleHistone Deacetylase InhibitorsRibonucleotide reductasemedicine.anatomical_structureTrichostatin AOncologychemistryApoptosisCancer researchSettore BIO/14 - FarmacologiaHistone deacetylaseReactive Oxygen Speciesmedicine.drug
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Role of exosomes released by chronic myelogenous leukemia cells in angiogenesis

2012

The present study is designed to assess if exosomes released from Chronic Myelogenous Leukemia (CML) cells may modulate angiogenesis. We have isolated and characterized the exosomes generated from LAMA84 CML cells and demonstrated that addition of exosomes to human vascular endothelial cells (HUVEC) induces an increase of both ICAM-1 and VCAM-1 cell adhesion molecules and interleukin-8 expression. The stimulation of cell-cell adhesion molecules was paralleled by a dose-dependent increase of adhesion of CML cells to a HUVEC monolayer. We further showed that the treatment with exosomes from CML cells caused an increase in endothelial cell motility accompanied by a loss of VE-cadherin and β-ca…

Cancer ResearchAngiogenesisVascular Cell Adhesion Molecule-1BiologyExosomesArticleExosomes Chronic Myelogenous Leukemia Cells Endothelial cells Tumor MicroenvironmentMiceAntigens CDCell Movementhemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineCell AdhesionHuman Umbilical Vein Endothelial CellsTumor MicroenvironmentAnimalsHumansCell adhesionbeta CateninMatrigelTumor microenvironmentNeovascularization PathologicCell adhesion moleculeInterleukin-8medicine.diseaseCadherinsIntercellular Adhesion Molecule-1MicrovesiclesCell biologyEndothelial stem cellDrug CombinationsOncologyGene Expression RegulationCancer researchProteoglycansCollagenLamininChronic myelogenous leukemia
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Crosstalk between leukemia-associated proteins MOZ and MLL regulates HOX gene expression in human cord blood CD34+ cells

2010

MOZ and MLL, encoding a histone acetyltransferase (HAT) and a histone methyltransferase, respectively, are targets for recurrent chromosomal translocations found in acute myeloblastic or lymphoblastic leukemia. In MOZ (MOnocytic leukemia Zinc-finger protein)/CBP- or mixed lineage leukemia (MLL)-rearranged leukemias, abnormal levels of HOX transcription factors have been found to be critical for leukemogenesis. We show that MOZ and MLL cooperate to regulate these key genes in human cord blood CD34+ cells. These chromatin-modifying enzymes interact, colocalize and functionally cooperate, and both are recruited to multiple HOX promoters. We also found that WDR5, an adaptor protein essential fo…

Cancer ResearchAntigens CD34HistonesHistone H3hemic and lymphatic diseasesHistone methylationGeneticsHumansWDR5Tissue DistributionPromoter Regions GeneticHox geneneoplasmsMolecular BiologyCells CulturedHistone AcetyltransferasesHomeodomain ProteinsGeneticsBlood CellsbiologyIntracellular Signaling Peptides and ProteinsHistone-Lysine N-MethyltransferaseReceptor Cross-TalkU937 CellsHistone acetyltransferaseFetal BloodHematopoiesisCell biologyGene Expression RegulationHistone methyltransferasebiology.proteinMyeloid-Lymphoid Leukemia ProteinH3K4me3K562 CellsMyeloid-Lymphoid Leukemia ProteinProtein BindingOncogene
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Patterns of Innate or Acquired Resistance to Anticancer Drugs: Our Experience to Overcome It

2021

Drug resistance, which is often of a multiple type, can be defined as the ability of cancer cells to obtain resistance to both conventional and novel chemotherapy agents. It remains a major problem to solve in cancer therapy. The mechanisms of resistance are multifactorial, and in our cellular models of acute myeloid leukemia, hepatocellular carcinoma, and triple-negative breast cancer, it involves the NF-κB pathway. In our opinion, multitarget molecules can be considered as privileged compounds capable of attacking and reversing the resistant phenotype. In the phenomena of both innate and acquired drug resistance that we have been studying since 1998 to today and up to 2016 under the guida…

Cancer ResearchAntineoplastic AgentsApoptosisPhosphatidylethanolamine Binding ProteinDrug resistanceMetastasisBreast cancerdrug resistance P-glycoprotein IAP NF-κBNeoplasmsHumansMedicineATP Binding Cassette Transporter Subfamily B Member 1Transcription factorYY1 Transcription FactorP-glycoproteinbiologybusiness.industryKinaseNF-kappa BMyeloid leukemiamedicine.diseaseDrug Resistance NeoplasmCancer cellSettore BIO/14 - Farmacologiabiology.proteinCancer researchbusinessCritical Reviews™ in Oncogenesis
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BCL2 gene polymorphisms and splicing variants in chronic myeloid leukemia.

2015

Recent data suggest that constitutional genetic variation in the antiapoptotic BCL2 gene could be associated with the susceptibility to develop chronic myeloid leukemia (CML) and the clinical outcome in several hematological malignancies. The present study examines whether BCL2 single nucleotide polymorphisms (SNPs) predispose to CML or may potentially influence the disease characteristics at diagnosis. Notably, no association was observed between the four candidate BCL2 SNPs and the risk of developing CML. Instead, the 4777C>A (rs2279115) and the 5735A>G (rs1801018) SNPs were significantly associated with the disease risk profile as determined by the Sokal score. We found that such polymor…

Cancer ResearchBCL2business.industryAlternative splicingChronic myeloid leukemiaClinical courseMyeloid leukemiaSingle-nucleotide polymorphismHematologyBioinformaticsSplicingBCL2 Chronic myeloid leukemia Polymorphisms Splicing SusceptibilityOncologyimmune system diseasesSusceptibilityhemic and lymphatic diseasesGenetic variationRNA splicingMedicinebiological phenomena cell phenomena and immunitySokal ScorebusinessPolymorphismsGeneneoplasms
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A new pericentric inv(8) in acute nonlymphocytic leukemia.

1993

Abstract Chromosome studies were carried out on unstimulated bone marrow cells from a patient with a diagnosis of acute nonlymphocytic leukemia (FAB M6 ANLL). Cytogenetic analysis revealed a mosaic chromosome pattern 46,XX46,XX,inv(8)(p21q24). This pericentric inversion has not been previously described in ANLL. Because, fragile sites, zinc finger gene loci, and the MYC protooncogene have been localized to band 8q24, a putative role for these sites and genes could be considered.

Cancer ResearchBiologychromosome Acute nonlymphocytic leukemia cytogeneticshemic and lymphatic diseasesGeneticsmedicineHumansMolecular BiologyGeneChromosomal inversionZinc fingerGeneticsChromosomal fragile siteChromosomeMiddle Agedmedicine.diseaseMolecular biologySettore BIO/18 - GeneticaLeukemiaLeukemia Myeloid Acutemedicine.anatomical_structureKaryotypingChromosome InversionFemaleBone marrowChromosomes Human Pair 8Cancer genetics and cytogenetics
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Novel pathway in Bcr-Abl signal transduction involves Akt-independent, PLC-γ1-driven activation of mTOR/p70S6-kinase pathway

2009

In chronic myeloid leukemia, activation of the phosphoinositide 3-kinase (PI3K)/Akt pathway is crucial for survival and proliferation of leukemic cells. Essential downstream molecules involve mammalian target of rapamycin (mTOR) and S6-kinase. Here, we present a comprehensive analysis of the molecular events involved in activation of these key signaling pathways. We provide evidence for a previously unrecognized phospholipase C-gamma1 (PLC-gamma1)-controlled mechanism of mTOR/p70S6-kinase activation, which operates in parallel to the classical Akt-dependent machinery. Short-term imatinib treatment of Bcr-Abl-positive cells caused dephosphorylation of p70S6-K and S6-protein without inactivat…

Cancer ResearchBlotting WesternMedizinFusion Proteins bcr-ablApoptosisProtein Serine-Threonine KinasesBiologyPiperazinesMiceLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesGeneticsAnimalsHumansRNA Small InterferingProtein Kinase InhibitorsMolecular BiologyProtein kinase BCAMKPI3K/AKT/mTOR pathwayPhospholipase C gammaCell growthKinaseTOR Serine-Threonine KinasesRPTORIntracellular Signaling Peptides and ProteinsRibosomal Protein S6 Kinases 70-kDaCell biologyEnzyme ActivationPyrimidinesBenzamidesembryonic structuresImatinib MesylateCancer researchPhosphorylationSignal transductionProto-Oncogene Proteins c-aktSignal TransductionOncogene
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Release of IFNγ by Acute Myeloid Leukemia Cells Remodels Bone Marrow Immune Microenvironment by Inducing Regulatory T Cells

2022

Abstract Purpose: The stromal and immune bone marrow (BM) landscape is emerging as a crucial determinant for acute myeloid leukemia (AML). Regulatory T cells (Treg) are enriched in the AML microenvironment, but the underlying mechanisms are poorly elucidated. Here, we addressed the effect of IFNγ released by AML cells in BM Treg induction and its impact on AML prognosis. Experimental Design: BM aspirates from patients with AML were subdivided according to IFNG expression. Gene expression profiles in INFγhigh and IFNγlow samples were compared by microarray and NanoString analysis and used to compute a prognostic index. The IFNγ release effect on the BM microenvironment was investigated in me…

Cancer ResearchBone Marrow CellsMesenchymal Stem CellsSettore MED/08 - Anatomia PatologicaT-Lymphocytes RegulatoryInterferon-gammaLeukemia Myeloid AcuteMiceOncologyBone Marrowhemic and lymphatic diseasesTumor MicroenvironmentAnimalsIFNγ Acute Myeloid Leukemia Bone Marrow Immune Microenvironment
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The effects of the macrocyclic lactone bryostatin-1 on leukemic cells in vitro.

1992

The macrocyclic lactone bryostatin-1 was found to exert in vitro antineoplastic activity against several leukemic cell lines, including human K562 erythroleukemia, HL60 promyelocytic leukemia, REH and MOLT-4 lymphoblastic leukemias, CCRFCEM lymphoma, KG-1 myeloid leukemia, and murine P388 lymphocytic leukemia. No statistically significant difference in sensitivity to bryostatin-1 was found between adriamycin-resistant P388 and K526 subclones and their sensitive counterparts. Freshly explanted clonogenic leukemic cells showed a variable sensitivity to bryostatin-1 in 10/12 tested samples. The IC50 of clonogenic leukemic cells was 4 × 10–3 M bryostatin-1, and that of normal marrow CFU-GM was…

Cancer ResearchBryostatin 1LymphomaHL60Antineoplastic AgentsAntileukemic agent030218 nuclear medicine & medical imaging03 medical and health scienceschemistry.chemical_compoundLactones0302 clinical medicinehemic and lymphatic diseasesmedicineTumor Cells CulturedHumansClonogenic assayTumor Stem Cell AssayLeukemiaChemistryMyeloid leukemiaGeneral Medicinemedicine.diseaseBryostatinsHaematopoiesisLeukemiaOncology030220 oncology & carcinogenesisCancer researchMacrolidesDrug Screening Assays AntitumorK562 cellsTumori
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Suppression of Mcl-1 via RNA interference sensitizes human hepatocellular carcinoma cells towards apoptosis induction

2006

Abstract Background Hepatocelluar carcinoma (HCC) is one of the most common cancers worldwide and a major cause of cancer-related mortality. HCC is highly resistant to currently available chemotherapeutic drugs. Defects in apoptosis signaling contribute to this resistance. Myeloid cell leukemia-1 (Mcl-1) is an anti-apoptotic member of the Bcl-2 protein family which interferes with mitochondrial activation. In a previous study we have shown that Mcl-1 is highly expressed in tissues of human HCC. In this study, we manipulated expression of the Mcl-1 protein in HCC cells by RNA interference and analyzed its impact on apoptosis sensitivity of HCC cells in vitro. Methods RNA interference was per…

Cancer ResearchCarcinoma HepatocellularMyeloidCellAntineoplastic AgentsApoptosisBiologylcsh:RC254-282RNA interferenceCell Line Tumorhemic and lymphatic diseasesGeneticsmedicineHumansneoplasmsLiver Neoplasmslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasedigestive system diseasesIn vitroNeoplasm ProteinsGene Expression Regulation NeoplasticLeukemiamedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2OncologyApoptosisHepatocellular carcinomaCancer researchMyeloid Cell Leukemia Sequence 1 ProteinRNA InterferenceStem cellResearch ArticleBMC Cancer
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