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  • 1
    Language: English
    In: Leukemia, 2014-05, Vol.28 (5), p.1132-1134
    Subject(s): Core Binding Factors - genetics ; Leukemia, Myeloid, Acute - diagnosis ; Prognosis ; Leukemia, Myeloid, Acute - pathology ; Humans ; Proto-Oncogene Proteins c-kit - genetics ; Mutation ; Leukemia, Myeloid, Acute - genetics ; Development and progression ; Transcription factors ; Genetic aspects ; Gene mutations ; Health aspects ; Leukemia in children ; Index Medicus
    ISSN: 0887-6924
    E-ISSN: 1476-5551
    Source: Nature Open Access
    Source: Academic Search Ultimate
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 2
    Language: English
    In: Leukemia, 2017-01, Vol.31 (1), p.18-25
    Description: Recurrent molecular markers have been routinely used in acute myeloid leukemia (AML) for risk assessment at diagnosis, whereas their post-induction monitoring still represents a debated issue. We evaluated the prognostic value and biological impact of minimal residual disease (MRD) and of the allelic ratio (AR) of FLT3-internal-tandem duplication (ITD) in childhood AML. We retrospectively screened 494 children with de novo AML for FLT3-ITD mutation, identifying 54 harboring the mutation; 51% of them presented high ITD-AR at diagnosis and had worse event-free survival (EFS, 19.2 versus 63.5% for low ITD-AR, 〈0.05). Forty-one percent of children with high levels of MRD after the 1st induction course, measured by a patient-specific real-time-PCR, had worse EFS (22.2 versus 59.4% in low-MRD patients, P〈0.05). Next, we correlated these parameters with gene expression, showing that patients with high ITD-AR or persistent MRD had characteristic expression profiles with deregulated genes involved in methylation and acetylation. Moreover, patients with high CyclinA1 expression presented an unfavorable EFS (20.3 versus 51.2% in low CyclinA1 group, P〈0.01). Our results suggest that ITD-AR levels and molecular MRD should be considered in planning clinical management of FLT3-ITD patients. Different transcriptional activation of epigenetic and oncogenic profiles may explain variability in outcome among these patients, for whom novel therapeutic approaches are desirable.
    Subject(s): fms-Like Tyrosine Kinase 3 - genetics ; Disease-Free Survival ; Leukemia, Myeloid, Acute - diagnosis ; Prognosis ; Epigenesis, Genetic - genetics ; Humans ; Child, Preschool ; Retrospective Studies ; Gene Expression Regulation, Leukemic ; Child ; Neoplasm, Residual - genetics ; Leukemia, Myeloid, Acute - genetics ; Molecular targeted therapy ; Gene mutations ; Gene expression ; Health aspects ; Innovations ; Index Medicus
    ISSN: 0887-6924
    E-ISSN: 1476-5551
    Source: Nature Open Access
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 3
    Language: English
    In: Leukemia, 2017-04, Vol.31 (4), p.974-977
    Subject(s): Daunorubicin - therapeutic use ; Prognosis ; Cytarabine - therapeutic use ; Humans ; Up-Regulation - genetics ; Methotrexate - therapeutic use ; Mutation - genetics ; Cyclophosphamide - therapeutic use ; Down-Regulation - genetics ; Nuclear Pore Complex Proteins - genetics ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; Mercaptopurine - therapeutic use ; Oncogene Proteins, Fusion - genetics ; Vincristine - therapeutic use ; Leukemia, Myeloid, Acute - drug therapy ; Biomarkers, Tumor - genetics ; Asparaginase - therapeutic use ; Prednisone - therapeutic use ; Leukemia, Myeloid, Acute - genetics ; Translocation, Genetic - genetics ; Index Medicus
    ISSN: 0887-6924
    E-ISSN: 1476-5551
    Source: Nature Open Access
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 4
    Language: English
    In: Leukemia, 2016-09-01, Vol.30 (9), p.1887
    Description: cAMP response element binding protein (CREB) is frequently overexpressed in acute myeloid leukemia (AML) and acts as a proto-oncogene; however, it is still debated whether such overactivation alone is able to induce leukemia as its pathogenetic downstream signaling is still unclear. We generated a zebrafish model overexpressing CREB in the myeloid lineage, which showed an aberrant regulation of primitive hematopoiesis, and in 79% of adult CREB-zebrafish a block of myeloid differentiation, triggering to a monocytic leukemia akin the human counterpart. Gene expression analysis of CREB-zebrafish revealed a signature of 20 differentially expressed human homologous CREB targets in common with pediatric AML. Among them, we demonstrated that CREB overexpression increased CCAAT-enhancer-binding protein-[delta] (C/EBP[delta]) levels to cause myeloid differentiation arrest, and the silencing of CREB-C/EBP[delta] axis restored myeloid terminal differentiation. Then, C/EBP[delta] overexpression was found to identify a subset of pediatric AML affected by a block of myeloid differentiation at monocytic stage who presented a significant higher relapse risk and the enrichment of aggressive signatures. Finally, this study unveils the aberrant activation of CREB-C/EBP[delta] axis concurring to AML onset by disrupting the myeloid cell differentiation process. We provide a novel in vivo model to perform high-throughput drug screening for AML cure improvement.
    Subject(s): Pediatrics ; Analysis ; Cyclic adenylic acid ; Genetic aspects ; Gene expression ; Cell differentiation ; Protein binding
    ISSN: 0887-6924
    E-ISSN: 1476-5551
    Source: Nature Open Access
    Source: Alma/SFX Local Collection
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  • 5
    Language: English
    In: Leukemia, 2008-12, Vol.22 (12), p.2217-2225
    Description: The inducible cyclic AMP (cAMP) early repressor (ICER) and cAMP response element-binding protein (CREB) are transcriptional regulators of the cAMP-mediated signaling pathway. CREB has been demonstrated to be upregulated in the majority of childhood leukemias contributing to disease progression, whereas ICER, its endogenous repressor, was found to be downregulated. Our research focus has been the function of restored ICER expression. ICER exogenously expressed in cell lines decreases CREB protein level and induces a lowered clonogenic potential in vitro. It decreases the ability of HL60 to invade the extramedullary sites and to promote bone marrow angiogenesis in nonobese diabetic-severe combined immunodeficient mice, demonstrating its potential effects on tumor progression. ICER represses the majority of 96 target genes upregulated by CREB. It binds CRE promoters and controls gene expression restoring the normal regulation of major cellular pathways. ICER is subjected to degradation through a constitutively active form of the extracellular signal-regulated protein kinase, which drives it to the proteasome. We propose that ICER is downregulated in HL60 to preserve CREB overexpression, which disrupts normal myelopoiesis and promotes blast proliferation. These findings define the function of ICER as a tumor suppressor in leukemia. Unbalanced CREB/ICER expression needs to be considered a pathogenetic feature in leukemogenesis. The molecular characterization of this pathway could be useful for novel therapeutic strategies.
    Subject(s): Hematologic and hematopoietic diseases ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Biological and medical sciences ; Medical sciences ; Neoplasm Transplantation ; Leukemia, Promyelocytic, Acute - pathology ; Jurkat Cells ; Humans ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Gene Expression Regulation, Leukemic ; Cyclic AMP Response Element Modulator - metabolism ; Mice, SCID ; Disease Progression ; Down-Regulation - physiology ; Phenotype ; Animals ; Cyclic AMP Response Element Modulator - genetics ; Leukemia, Promyelocytic, Acute - physiopathology ; Cyclic AMP Response Element-Binding Protein - metabolism ; HL-60 Cells ; Mice, Inbred NOD ; Blast Crisis - genetics ; Mice ; HeLa Cells ; Leukemia, Promyelocytic, Acute - genetics ; Proteasome Endopeptidase Complex - metabolism ; Care and treatment ; Proteolysis ; Leukemia ; Physiological aspects ; Genetic aspects ; DNA binding proteins ; Research ; Gene expression ; Index Medicus
    ISSN: 0887-6924
    E-ISSN: 1476-5551
    Source: Nature Open Access
    Source: Academic Search Ultimate
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 6
    Language: English
    In: Genetics and molecular research, 2017, Vol.16 (3)
    ISSN: 1676-5680
    E-ISSN: 1676-5680
    Source: Alma/SFX Local Collection
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  • 7
    Language: English
    In: Cancer research (Chicago, Ill.), 2009, Vol.69 (6), p.2471-2478
    Description: The cyclic AMP-responsive element binding protein (CREB) is documented to be overexpressed in leukemia, but the underlying mechanism remains unknown. Here, microRNAs (miRNA), which act as negative regulators of gene expression principally through translational repression, are investigated for the mediation of high CREB protein levels. A series of miRNAs that target CREB were identified. Real-time quantitative PCR revealed that miR-34b was expressed significantly less in myeloid cell lines, previously known for high CREB protein levels. Exogenous miR-34b expression was induced, and results revealed a direct interaction with the CREB 3'-untranslated region, with the consequent reduction of the CREB protein levels in vitro. miR-34b restored expression caused cell cycle abnormalities, reduced anchorage-independent growth, and altered CREB target gene expression, suggesting its suppressor potential. Using reverse-phase protein array, CREB target proteins (BCL-2, cyclin A1, cyclin B1, cyclin D, nuclear factor-kappaB, Janus-activated kinase 1, and signal transducer and activator of transcription 3), as well as many downstream protein kinases and cell survival signaling pathways (AKT/mammalian target of rapamycin and extracellular signal-regulated kinase) usually elicited by CREB, were observed to have decreased. The miR-34b/miR-34c promoter was shown to be methylated in the leukemia cell lines used. This epigenetic regulation should control the observed miR-34b expression levels to maintain the CREB protein overexpressed. In addition, the inverse correlation between miR-34b and CREB expression was found in a cohort of 78 pediatric patients at diagnosis of acute myeloid leukemia, supporting this relationship in vivo. Our results identify a direct miR-34b target gene, provide a possible mechanism for CREB overexpression, and provide new information about myeloid transformation and therapeutic strategies.
    Subject(s): Hematologic and hematopoietic diseases ; Pharmacology. Drug treatments ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Biological and medical sciences ; Medical sciences ; Antineoplastic agents ; Tumors ; Promoter Regions, Genetic ; RNA, Small Interfering - genetics ; Acute Disease ; Cyclic AMP Response Element-Binding Protein - biosynthesis ; Gene Expression ; Humans ; Leukemia, Myeloid - genetics ; MicroRNAs - biosynthesis ; Leukemia, Myeloid - pathology ; Cyclic AMP Response Element-Binding Protein - genetics ; DNA Methylation ; Transfection ; Leukemia, Myeloid - metabolism ; Cell Line, Tumor ; HL-60 Cells ; Transcription, Genetic ; MicroRNAs - genetics ; 3' Untranslated Regions ; Cell Growth Processes - genetics ; Index Medicus
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: HighWire Press (Free Journals)
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 8
    Language: English
    In: Leukemia, 2016-09, Vol.30 (9), p.1887-1896
    Description: cAMP response element binding protein (CREB) is frequently overexpressed in acute myeloid leukemia (AML) and acts as a proto-oncogene; however, it is still debated whether such overactivation alone is able to induce leukemia as its pathogenetic downstream signaling is still unclear. We generated a zebrafish model overexpressing CREB in the myeloid lineage, which showed an aberrant regulation of primitive hematopoiesis, and in 79% of adult CREB-zebrafish a block of myeloid differentiation, triggering to a monocytic leukemia akin the human counterpart. Gene expression analysis of CREB-zebrafish revealed a signature of 20 differentially expressed human homologous CREB targets in common with pediatric AML. Among them, we demonstrated that CREB overexpression increased CCAAT-enhancer-binding protein-δ (C/EBPδ) levels to cause myeloid differentiation arrest, and the silencing of CREB-C/EBPδ axis restored myeloid terminal differentiation. Then, C/EBPδ overexpression was found to identify a subset of pediatric AML affected by a block of myeloid differentiation at monocytic stage who presented a significant higher relapse risk and the enrichment of aggressive signatures. Finally, this study unveils the aberrant activation of CREB-C/EBPδ axis concurring to AML onset by disrupting the myeloid cell differentiation process. We provide a novel in vivo model to perform high-throughput drug screening for AML cure improvement.
    Subject(s): Zebrafish ; Leukemia, Myeloid, Acute - etiology ; Carcinogenesis ; Myeloid Cells ; Cell Lineage ; Cyclic AMP Response Element-Binding Protein - genetics ; Monocytes ; Animals ; Hematopoiesis ; Cyclic AMP Response Element-Binding Protein - metabolism ; CCAAT-Enhancer-Binding Protein-delta - metabolism ; Cell Differentiation ; Disease Models, Animal ; Index Medicus
    ISSN: 0887-6924
    E-ISSN: 1476-5551
    Source: Nature Open Access
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 9
    Language: English
    In: Haematologica (Roma), 2013-04-01, Vol.98 (4), p.602-610
    Description: MicroRNA-34b down-regulation in acute myeloid leukemia was previously shown to induce CREB overexpression, thereby causing leukemia proliferation in vitro and in vivo. The role of microRNA-34b and CREB in patients with myeloid malignancies has never been evaluated. We examined microRNA-34b expression and the methylation status of its promoter in cells from patients diagnosed with myeloid malignancies. We used gene expression profiling to identify signatures of myeloid transformation. We established that microRNA-34b has suppressor ability and that CREB has oncogenic potential in primary bone marrow cell cultures and in vivo. MicroRNA-34b was found to be up-regulated in pediatric patients with juvenile myelomonocytic leukemia (n=17) and myelodysplastic syndromes (n=28), but was down-regulated in acute myeloid leukemia patients at diagnosis (n=112). Our results showed that hypermethylation of the microRNA-34b promoter occurred in 66% of cases of acute myeloid leukemia explaining the low microRNA-34b levels and CREB overexpression, whereas preleukemic myelodysplastic syndromes and juvenile myelomonocytic leukemia were not associated with hypermethylation or CREB overexpression. In paired samples taken from the same patients when they had myelodysplastic syndrome and again during the subsequent acute myeloid leukemia, we confirmed microRNA-34b promoter hypermethylation at leukemia onset, with 103 CREB target genes differentially expressed between the two disease stages. This subset of CREB targets was confirmed to associate with high-risk myelodysplastic syndromes in a separate cohort of patients (n=20). Seventy-eight of these 103 CREB targets were also differentially expressed between healthy samples (n=11) and de novo acute myeloid leukemia (n=72). Further, low microRNA-34b and high CREB expression levels induced aberrant myelopoiesis through CREB-dependent pathways in vitro and in vivo. In conclusion, we suggest that microRNA-34b controls CREB expression and contributes to myeloid transformation from both healthy bone marrow and myelodysplastic syndromes. We identified a subset of CREB target genes that represents a novel transcriptional network that may control myeloid transformation.
    Subject(s): Humans ; Leukemia, Myeloid - genetics ; Child, Preschool ; Infant ; Gene Expression Profiling ; Promoter Regions, Genetic - genetics ; DNA Methylation ; Cell Transformation, Neoplastic - genetics ; Child ; Infant, Newborn ; Acute Disease ; Cells, Cultured ; Gene Expression Regulation, Leukemic ; Mice, SCID ; Interleukin Receptor Common gamma Subunit - genetics ; Mice, Knockout ; Interleukin Receptor Common gamma Subunit - deficiency ; Cyclic AMP Response Element-Binding Protein - genetics ; Animals ; Adolescent ; HL-60 Cells ; Myeloid Cells - metabolism ; Mice, Inbred NOD ; Mice ; MicroRNAs - genetics ; Myelodysplastic Syndromes - genetics ; Myeloid Cells - pathology ; Index Medicus ; Original and Brief Reports
    ISSN: 0390-6078
    E-ISSN: 1592-8721
    Source: HighWire Press (Free Journals)
    Source: PubMed Central
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 10
    Language: English
    In: Journal of materials science, 2015-03, Vol.50 (5), p.2202-2217
    Description: Recrystallization of a ball-milled ferritic ODS steel is studied towards its evolution from as-milled powder to consolidated state. This characterization has been made possible by using a combination of X-ray Diffraction (XRD) and an innovative method based on an Automated Crystallographic Orientation Mapping (ACOM) tool attached to a Transmission Electron Microscope (TEM). Focus Ion Beam preparation has been essential to obtain a thin section of the ODS steel powder particle and perform the ACOM-TEM study. Relevant temperatures regarding recovery and recrystallization during the heat treatment had first been identified with XRD profile analysis. Selected states were further characterized using ACOM-TEM that provides key information on microstructure, i.e. grain size and morphology, crystallite size, local texture and distortion. ACOM-TEM cartographies have revealed for the first time that the microstructure of as-milled ODS ferritic steel particles consists in very anisotropic grains containing undistorted domains and dislocation walls. This is in agreement with the nanosized crystallites measured by XRD results. The mutual benefits of XRD and ACOM-TEM methods to analyse and describe the microstructure are discussed as well as the reliability of dislocation density measurements provided by ACOM-TEM misorientation measurements. In addition, of the ACOM-TEM results, the microstructural evolution during the processing route is interpreted in terms of a competition between recovery, recrystallization, grain growth and precipitation.
    Subject(s): Polymer Sciences ; Materials Science, general ; Mechanics ; Characterization and Evaluation of Materials ; Material Science ; Continuum Mechanics and Mechanics of Materials ; Crystallography ; Powders ; Diffraction ; Precipitation (Meteorology) ; Transmission electron microscopes ; X-rays ; Grain size ; Dispersion hardening steels ; Cartography ; Heat treatment ; Grain growth ; Domain walls ; Ball milling ; X-ray diffraction ; Ferritic stainless steels ; Mapping ; Recovery ; Ion beams ; Dislocation density ; Domains ; Crystallites ; Transmission electron microscopy ; Misalignment ; Morphology ; Recrystallization ; Evolution ; Microstructure ; Material chemistry ; Chemical Sciences
    ISSN: 0022-2461
    E-ISSN: 1573-4803
    Source: Academic Search Ultimate
    Source: Alma/SFX Local Collection
    Source: ProQuest Central
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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