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[PMID]:28886412
[Au] Autor:Chen Y; Pourabdollah M; Atenafu EG; Tierens A; Schimmer A; Chang H
[Ad] Endereço:Department of Laboratory Hematology, Laboratory Medicine Program, University Health Network, University of Toronto, Toronto, Canada; The First Affiliated Hospital of Nanchang University, Nanchang, China.
[Ti] Título:Re-evaluation of acute erythroid leukemia according to the 2016 WHO classification.
[So] Source:Leuk Res;61:39-43, 2017 Oct.
[Is] ISSN:1873-5835
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In the recent update of WHO classification, the definition of myeloid neoplasms with erythroid predominance has been modified shifting the main criteria for calculating blast percentage from non-erythroid cells (NEC) to all nucleated marrow cells (ANC). Thus, the cases previously classified as erythroid/myeloid subtype of acute erythroid leukemia (AEL) based on the 2008 WHO will now be categorized either as myelodysplastic syndrome with excess blasts (MDS-EB) or acute myeloid leukemia, not otherwise specified (AML-NOS). However, the clinical significance of this new classification has not been demonstrated. Thus, we reviewed a leukemia database and reclassified 38 cases previously diagnosed as AEL, erythroid/myeloid subtype, with the consideration of 2016 revision criteria. Twenty seven (71%) of them had >20% blasts in NEC but less than 20% blasts in ANC, and 11 (29%) had >20% in both NEC and ANC. There was no significant difference in overall survivals (OS) among AEL, MDS-EB, and AML-NOS (non-erythroid predominance, NEP). However, AML with myelodysplasia-related changes showed significant shorter OS than AEL, MDS-EB and AML-NOS (NEP). Our results indicate that in myeloid neoplasm with erythroid predominance, patients with >20% blasts, of either NEC or ANC, share similar clinical laboratory features and survival outcomes with AML-NOS.
[Mh] Termos MeSH primário: Leucemia Eritroblástica Aguda/classificação
Leucemia Eritroblástica Aguda/diagnóstico
Leucemia Eritroblástica Aguda/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Feminino
Seres Humanos
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Modelos de Riscos Proporcionais
Organização Mundial da Saúde
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


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[PMID]:28802832
[Au] Autor:Streltsova MA; Barsov E; Erokhina SA; Kovalenko EI
[Ad] Endereço:Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, ul. Miklukho-Maklaya, Moscow 117997, Russia. Electronic address: mstreltsova@mail.ru.
[Ti] Título:Retroviral gene transfer into primary human NK cells activated by IL-2 and K562 feeder cells expressing membrane-bound IL-21.
[So] Source:J Immunol Methods;450:90-94, 2017 Nov.
[Is] ISSN:1872-7905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Natural killer (NK) cells are capable of rapidly recognizing and efficiently killing tumor cells. This makes them a potentially promising agent for cancer immunotherapy. Additional genetic modifications of NK cells may further improve their anti-tumor efficacy. Numerous technical challenges associated with gene delivery into NK cells have significantly tempered this approach. We achieved efficient retroviral vector transduction of primary human NK cells that were stimulated by a combination of IL-2 and engineered K562 cells expressing membrane-bound IL-21. The activated NK cells were in less differentiated state and expressed NK cell activation receptors NKG2D, NKp30, CD16, and were highly HLA-DR-positive. This NK cell population was highly susceptible to the transduction by both GFP- and NGFR-expressing retroviral vectors, with transduction efficiency exceeding 50%. More mature CD57 NK cell population was generally resistant to retroviral vector transduction because of poor response to the stimulation. Our findings may facilitate retroviral vector-mediated genetic engineering of human primary NK cells for future immunotherapies.
[Mh] Termos MeSH primário: Vetores Genéticos
Imunoterapia/métodos
Interleucina-2/metabolismo
Interleucinas/metabolismo
Células Matadoras Naturais/metabolismo
Leucemia Eritroblástica Aguda/terapia
Ativação Linfocitária
Retroviridae/genética
Transdução Genética
Transfecção/métodos
[Mh] Termos MeSH secundário: Antígenos CD57/imunologia
Antígenos CD57/metabolismo
Diferenciação Celular
Técnicas de Cocultura
Células Alimentadoras
Proteínas Ligadas por GPI/imunologia
Proteínas Ligadas por GPI/metabolismo
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Antígenos HLA-DR/imunologia
Antígenos HLA-DR/metabolismo
Seres Humanos
Interleucina-2/imunologia
Interleucinas/imunologia
Células Jurkat
Células K562
Células Matadoras Naturais/imunologia
Leucemia Eritroblástica Aguda/genética
Leucemia Eritroblástica Aguda/imunologia
Leucemia Eritroblástica Aguda/metabolismo
Subfamília K de Receptores Semelhantes a Lectina de Células NK/imunologia
Subfamília K de Receptores Semelhantes a Lectina de Células NK/metabolismo
Receptor 3 Desencadeador da Citotoxicidade Natural/imunologia
Receptor 3 Desencadeador da Citotoxicidade Natural/metabolismo
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Receptores de IgG/imunologia
Receptores de IgG/metabolismo
Receptores de Fator de Crescimento Neural/genética
Receptores de Fator de Crescimento Neural/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD57 Antigens); 0 (FCGR3B protein, human); 0 (GPI-Linked Proteins); 0 (HLA-DR Antigens); 0 (Interleukin-2); 0 (Interleukins); 0 (KLRK1 protein, human); 0 (NCR3 protein, human); 0 (NGFR protein, human); 0 (NK Cell Lectin-Like Receptor Subfamily K); 0 (Natural Cytotoxicity Triggering Receptor 3); 0 (Nerve Tissue Proteins); 0 (Receptors, IgG); 0 (Receptors, Nerve Growth Factor); 0 (interleukin-21); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170814
[St] Status:MEDLINE


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[PMID]:28676717
[Au] Autor:Chen Z; Xu X; Ren J; Wang W; Liu X; Li E
[Ad] Endereço:School of Ocean Sciences, China University of Geosciences, Beijing, People's Republic of China.
[Ti] Título:Trichopeptides A and B, trichocyclodipeptides A-C, new peptides from the ascomycete fungus Stagonospora trichophoricola.
[So] Source:J Antibiot (Tokyo);70(9):923-928, 2017 Aug.
[Is] ISSN:0021-8820
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Trichopeptides A (1) and B (2), new linear tetrapeptide and tripeptide, respectively, and three new diketopiperazines trichocyclodipeptides A-C (3-5) were isolated from the fermentation of the ascomycete fungus Stagonospora trichophoricola, a fungus isolated from the soil sample surrounding the fruiting body of Ophiocordyceps sinensis in Maqin Country, Qinghai Province, People's Republic of China. Their structures were primarily elucidated by interpretation of NMR and MS experiments. The absolute configurations of 1-5 were assigned through Marfey's method on their acid hydrolyzates. Compound 3 showed antifungal activity against Candida albicans with the IC and MIC values of 22 and 90 µg ml , respectively.
[Mh] Termos MeSH primário: Antibacterianos/isolamento & purificação
Antibióticos Antineoplásicos/isolamento & purificação
Antifúngicos/isolamento & purificação
Peptídeos Catiônicos Antimicrobianos/isolamento & purificação
Ascomicetos/metabolismo
Descoberta de Drogas
[Mh] Termos MeSH secundário: Células A549
Adenocarcinoma Bronquíolo-Alveolar/tratamento farmacológico
Sequência de Aminoácidos
Antibacterianos/química
Antibacterianos/farmacologia
Antibióticos Antineoplásicos/química
Antibióticos Antineoplásicos/farmacologia
Antifúngicos/química
Antifúngicos/farmacologia
Peptídeos Catiônicos Antimicrobianos/química
Peptídeos Catiônicos Antimicrobianos/farmacologia
Bacillus subtilis/efeitos dos fármacos
Bacillus subtilis/crescimento & desenvolvimento
Candida albicans/efeitos dos fármacos
Candida albicans/crescimento & desenvolvimento
Sobrevivência Celular/efeitos dos fármacos
Escherichia coli/efeitos dos fármacos
Escherichia coli/crescimento & desenvolvimento
Fermentação
Seres Humanos
Concentração Inibidora 50
Células K562
Leucemia Eritroblástica Aguda/tratamento farmacológico
Testes de Sensibilidade Microbiana
Oligopeptídeos/química
Oligopeptídeos/isolamento & purificação
Oligopeptídeos/farmacologia
Staphylococcus aureus/efeitos dos fármacos
Staphylococcus aureus/crescimento & desenvolvimento
Estereoisomerismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Antibiotics, Antineoplastic); 0 (Antifungal Agents); 0 (Antimicrobial Cationic Peptides); 0 (Oligopeptides); 0 (trichocyclodipeptide A); 0 (trichocyclodipeptide B); 0 (trichocyclodipeptide C); 0 (trichopeptide A); 0 (trichopeptide B)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170706
[St] Status:MEDLINE
[do] DOI:10.1038/ja.2017.76


  4 / 5574 MEDLINE  
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[PMID]:28652408
[Au] Autor:Hirbawi J; Bialkowska K; Bledzka KM; Liu J; Fukuda K; Qin J; Plow EF
[Ad] Endereço:From the Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195.
[Ti] Título:The extreme C-terminal region of kindlin-2 is critical to its regulation of integrin activation.
[So] Source:J Biol Chem;292(34):14258-14269, 2017 Aug 25.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kindlin-2 (K2), a 4.1R-ezrin-radixin-moesin (FERM) domain adaptor protein, mediates numerous cellular responses, including integrin activation. The C-terminal 15-amino acid sequence of K2 is remarkably conserved across species but is absent in canonical FERM proteins, including talin. In CHO cells expressing integrin αIIbß3, co-expression of K2 with talin head domain resulted in robust integrin activation, but this co-activation was lost after deletion of as few as seven amino acids from the K2 C terminus. This dependence on the C terminus was also observed in activation of endogenous αIIbß3 in human erythroleukemia (HEL) cells and ß1 integrin activation in macrophage-like RAW264.1 cells. Kindlin-1 (K1) exhibited a similar dependence on its C terminus for integrin activation. Expression of the K2 C terminus as an extension of membrane-anchored P-selectin glycoprotein ligand-1 (PSGL-1) inhibited integrin-dependent cell spreading. Deletion of the K2 C terminus did not affect its binding to the integrin ß3 cytoplasmic tail, but combined biochemical and NMR analyses indicated that it can insert into the F2 subdomain. We suggest that this insertion determines the topology of the K2 FERM domain, and its deletion may affect the positioning of the membrane-binding functions of the F2 subdomain and the integrin-binding properties of its F3 subdomain. Free C-terminal peptide can still bind to K2 and displace the endogenous K2 C terminus but may not restore the conformation needed for integrin co-activation. Our findings indicate that the extreme C terminus of K2 is essential for integrin co-activation and highlight the importance of an atypical architecture of the K2 FERM domain in regulating integrin activation.
[Mh] Termos MeSH primário: Integrina alfa2/metabolismo
Integrina beta3/metabolismo
Leucemia Eritroblástica Aguda/metabolismo
Macrófagos/metabolismo
Proteínas de Membrana/metabolismo
Proteínas de Neoplasias/metabolismo
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Animais
Células CHO
Linhagem Celular Tumoral
Cricetulus
Deleção de Genes
Seres Humanos
Integrina alfa2/química
Integrina alfa2/genética
Integrina beta3/química
Integrina beta3/genética
Leucemia Eritroblástica Aguda/patologia
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Macrófagos/citologia
Proteínas de Membrana/química
Proteínas de Membrana/genética
Camundongos
Mutação
Proteínas de Neoplasias/agonistas
Proteínas de Neoplasias/química
Proteínas de Neoplasias/genética
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Domínios e Motivos de Interação entre Proteínas
Multimerização Proteica
Células RAW 264.7
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Proteínas Recombinantes/química
Proteínas Recombinantes/metabolismo
Talina/química
Talina/genética
Talina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ITGA2B protein, human); 0 (ITGB3 protein, human); 0 (Integrin alpha2); 0 (Integrin beta3); 0 (Luminescent Proteins); 0 (MIG2B protein, human); 0 (Membrane Proteins); 0 (Neoplasm Proteins); 0 (Peptide Fragments); 0 (Recombinant Fusion Proteins); 0 (Recombinant Proteins); 0 (Talin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.776195


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[PMID]:28520978
[Au] Autor:Krivega I; Dean A
[Ad] Endereço:Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
[Ti] Título:LDB1-mediated enhancer looping can be established independent of mediator and cohesin.
[So] Source:Nucleic Acids Res;45(14):8255-8268, 2017 Aug 21.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mechanistic studies in erythroid cells indicate that LDB1, as part of a GATA1/TAL1/LMO2 complex, brings erythroid-expressed genes into proximity with enhancers for transcription activation. The role of co-activators in establishing this long-range interaction is poorly understood. Here we tested the contributions of the RNA Pol II pre-initiation complex (PIC), mediator and cohesin to establishment of locus control region (LCR)/ß-globin proximity. CRISPR/Cas9 editing of the ß-globin promoter to eliminate the RNA Pol II PIC by deleting the TATA-box resulted in loss of transcription, but enhancer-promoter interaction was unaffected. Additional deletion of the promoter GATA1 site eliminated LDB1 complex and mediator occupancy and resulted in loss of LCR/ß-globin proximity. To separate the roles of LDB1 and mediator in LCR looping, we expressed a looping-competent but transcription-activation deficient form of LDB1 in LDB1 knock down cells: LCR/ß-globin proximity was restored without mediator core occupancy. Further, Cas9-directed tethering of mutant LDB1 to the ß-globin promoter forced LCR loop formation in the absence of mediator or cohesin occupancy. Moreover, ENCODE data and our chromatin immunoprecipitation results indicate that cohesin is almost completely absent from validated and predicted LDB1-regulated erythroid enhancer-gene pairs. Thus, lineage specific factors largely mediate enhancer-promoter looping in erythroid cells independent of mediator and cohesin.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/genética
Proteínas Cromossômicas não Histona/genética
Proteínas de Ligação a DNA/genética
Elementos Facilitadores Genéticos/genética
Regulação Leucêmica da Expressão Gênica
Proteínas com Domínio LIM/genética
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Western Blotting
Sistemas CRISPR-Cas
Proteínas de Ciclo Celular/metabolismo
Linhagem Celular Tumoral
Proteínas Cromossômicas não Histona/metabolismo
Proteínas de Ligação a DNA/metabolismo
Proteínas com Domínio LIM/metabolismo
Leucemia Eritroblástica Aguda/genética
Leucemia Eritroblástica Aguda/metabolismo
Leucemia Eritroblástica Aguda/patologia
Região de Controle de Locus Gênico/genética
Camundongos
Regiões Promotoras Genéticas/genética
RNA Polimerase II/genética
RNA Polimerase II/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Globinas beta/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Chromosomal Proteins, Non-Histone); 0 (DNA-Binding Proteins); 0 (LIM Domain Proteins); 0 (Ldb1 protein, mouse); 0 (beta-Globins); 0 (cohesins); EC 2.7.7.- (RNA Polymerase II)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx433


  6 / 5574 MEDLINE  
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[PMID]:28420120
[Au] Autor:Almeida AM; Prebet T; Itzykson R; Ramos F; Al-Ali H; Shammo J; Pinto R; Maurillo L; Wetzel J; Musto P; Van De Loosdrecht AA; Costa MJ; Esteves S; Burgstaller S; Stauder R; Autzinger EM; Lang A; Krippl P; Geissler D; Falantes JF; Pedro C; Bargay J; Deben G; Garrido A; Bonanad S; Diez-Campelo M; Thepot S; Ades L; Sperr WR; Valent P; Fenaux P; Sekeres MA; Greil R; Pleyer L
[Ad] Endereço:Instituto Português de Oncologia de Lisboa (IPOL), 1200-795 Lisbon, Portugal. amalmeida@ipolisboa.min-saude.pt.
[Ti] Título:Clinical Outcomes of 217 Patients with Acute Erythroleukemia According to Treatment Type and Line: A Retrospective Multinational Study.
[So] Source:Int J Mol Sci;18(4), 2017 Apr 14.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Acute erythroleukemia (AEL) is a rare disease typically associated with a poor prognosis. The median survival ranges between 3-9 months from initial diagnosis. Hypomethylating agents (HMAs) have been shown to prolong survival in patients with myelodysplastic syndromes (MDS) and AML, but there is limited data of their efficacy in AEL. We collected data from 210 AEL patients treated at 28 international sites. Overall survival (OS) and PFS were estimated using the Kaplan-Meier method and the log-rank test was used for subgroup comparisons. Survival between treatment groups was compared using the Cox proportional hazards regression model. Eighty-eight patients were treated with HMAs, 44 front line, and 122 with intensive chemotherapy (ICT). ICT led to a higher overall response rate (complete or partial) compared to first-line HMA (72% vs. 46.2%, respectively; ≤ 0.001), but similar progression-free survival (8.0 vs. 9.4 months; = 0.342). Overall survival was similar for ICT vs. HMAs (10.5 vs. 13.7 months; = 0.564), but patients with high-risk cytogenetics treated with HMA first-line lived longer (7.5 for ICT vs. 13.3 months; = 0.039). Our results support the therapeutic value of HMA in AEL.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Leucemia Eritroblástica Aguda/tratamento farmacológico
Leucemia Eritroblástica Aguda/mortalidade
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Azacitidina/administração & dosagem
Azacitidina/análogos & derivados
Biomarcadores
Medula Óssea/patologia
Análise Citogenética
Feminino
Seres Humanos
Leucemia Eritroblástica Aguda/diagnóstico
Masculino
Meia-Idade
Modelos de Riscos Proporcionais
Estudos Retrospectivos
Análise de Sobrevida
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Biomarkers); 776B62CQ27 (decitabine); M801H13NRU (Azacitidine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE


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[PMID]:28364352
[Au] Autor:Wang LP; Zhao YN; Sun X; Gao RL
[Ad] Endereço:College of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
[Ti] Título:Effects of bufalin on up-regulating methylation of Wilm's tumor 1 gene in human erythroid leukemic cells.
[So] Source:Chin J Integr Med;23(4):288-294, 2017 Apr.
[Is] ISSN:1672-0415
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To explore the effects of bufalin on inhibiting proliferation, up-regulating methylation of Wilm' tumor 1 gene (WT1) as well as its possible mechanisms in human erythroid leukemic (HEL) cells. METHODS: The HEL cells were treated with bufalin at various concentrations to observe cellular morphology, proliferation assay and cell cycle. The mRNA and protein expression levels of WT1 were detected by reverse transcription polymerase chain reaction (RT-PCR), Western blot and immunocytochemistry, DNA methylation of WT1 and protein expression levels of DNA methyltransferase 3a (DNMT3a) and DNMT3b were analyzed by methylation-specific PCR, and Western blot respectively. RESULTS: The bufalin was effective to inhibit proliferation of HEL cells in a dose-dependent manner, their suppression rates were from 23.4%±2.1% to 87.2%±5.4% with an half maximal inhibit concentration (IC ) of 0.046 µmol/L. Typical apoptosis morphology was observed in bufalin-treated HEL cells. The proliferation index of cell cycle decreased from 76.4%±1.9% to 49.7%±1.3%. The expression levels of WT1 mRNA and its protein reduced gradually with increasing doses of bufalin, meanwhile, the methylation status of WT1 gene changed from unmethylated into partially or totally methylated. While, the expression levels of DNMT3a and DNMT3b protein gradually increased by bufalin treatment in a dose-dependent manner. CONCLUSIONS: Bufalin can not only significantly inhibit the proliferation of HEL cells and arrest cell cycle at G /G phase, but also induce cellular apoptosis and down-regulate the expression level of WT1. Our results provide the evidence of bufalin for anti-leukemia, its mechanism may involve in increasing WT1 methylation status which is related to the up-regulation of DNMT3a and DNMT3b proteins in erythroid leukemic HEL cells.
[Mh] Termos MeSH primário: Bufanolídeos/farmacologia
Metilação de DNA/efeitos dos fármacos
Leucemia Eritroblástica Aguda/genética
Regulação para Cima/efeitos dos fármacos
Proteínas WT1/genética
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Apoptose/genética
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Forma Celular/efeitos dos fármacos
DNA (Citosina-5-)-Metiltransferases/metabolismo
Metilação de DNA/genética
Regulação Leucêmica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Leucemia Eritroblástica Aguda/enzimologia
Leucemia Eritroblástica Aguda/patologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Regulação para Cima/genética
Proteínas WT1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bufanolides); 0 (RNA, Messenger); 0 (WT1 Proteins); 0 (WT1 protein, human); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferases); EC 2.1.1.37 (DNA methyltransferase 3A); EC 2.1.1.37 (DNA methyltransferase 3B); U549S98QLW (bufalin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170402
[St] Status:MEDLINE
[do] DOI:10.1007/s11655-017-2404-1


  8 / 5574 MEDLINE  
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[PMID]:28359056
[Au] Autor:Zhu LF; Chen QR; Chen SZ; Wang LY; Luo XF; Ren JH; Yuan XH; Wu XQ; Zeng YL; Xiao M; Chen YQ; Chen YY; Lin MH; Wu ZJ; Chen ZZ; Hu JD; Yang T
[Ad] Endereço:Department of Hematology, Fujian Institute of Hematology, Fujian Provincial Key Laboratory of Hematology, Fujian Medical University Union Hospital, Fuzhou, China.
[Ti] Título:The Construction and Identification of Induced Pluripotent Stem Cells Derived from Acute Myelogenous Leukemia Cells.
[So] Source:Cell Physiol Biochem;41(4):1661-1674, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The present study aimed to establish an induced pluripotent stem cell (iPSC) line from acute myelogenous leukemia (AML) cells in vitro and identify their biological characteristics. METHODS: Cells from the AML-infiltrated skin from an M6 patient were infected with a lentivirus carrying OCT4, SOX2, KLF4 and C-MYC to induce iPSCs. The characteristics of the iPSCs were confirmed by alkaline phosphatase (ALP) staining. The proliferation ability of iPSCs was detected with a CCK-8 assay. The expression of pluripotency markers was measured by immunostaining, and the expression of stem cell-related genes was detected by qRT-PCR; distortion during the induction process was detected by karyotype analysis; the differentiation potential of iPSCs was determined by embryoid body-formation and teratoma-formation assays. ALP staining confirmed that these cells exhibited positive staining and had the characteristics of iPSCs. RESULTS: The CCK-8 assay showed that the iPSCs had the ability to proliferate. Immunostaining demonstrated that iPSC clones showed positive expression of NANOG, SSEA-3, SSEA-4, TRA-1-60 and TRA-1-81. qRT-PCR results revealed that the mRNA expression of Nanog, Lin28, Cripto, FOX3, DNMT3b, DPPA2, and DPPA4 significantly increased in iPSCs. Karyotype analysis found no chromosome aberration in the iPSCs. The results of the embryoid body-formation and teratoma-formation assays indicated that the iPSCs had the potential to differentiate into all three germ layers. CONCLUSION: Our study provided evidence that an iPSC line derived from AML cells was successfully established.
[Mh] Termos MeSH primário: Regulação Leucêmica da Expressão Gênica
Células-Tronco Pluripotentes Induzidas/metabolismo
Leucemia Eritroblástica Aguda/metabolismo
Proteínas de Neoplasias/biossíntese
Neoplasias Cutâneas/metabolismo
Fatores de Transcrição/biossíntese
[Mh] Termos MeSH secundário: Adulto
Seres Humanos
Células-Tronco Pluripotentes Induzidas/patologia
Leucemia Eritroblástica Aguda/genética
Leucemia Eritroblástica Aguda/patologia
Masculino
Proteínas de Neoplasias/genética
Neoplasias Cutâneas/genética
Neoplasias Cutâneas/patologia
Fatores de Transcrição/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neoplasm Proteins); 0 (Transcription Factors)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170621
[Lr] Data última revisão:
170621
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.1159/000471246


  9 / 5574 MEDLINE  
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[PMID]:28340113
[Au] Autor:Lee WY; Weinberg OK; Pinkus GS
[Ad] Endereço:From the Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
[Ti] Título:GATA1 Is a Sensitive and Specific Nuclear Marker for Erythroid and Megakaryocytic Lineages.
[So] Source:Am J Clin Pathol;147(4):420-426, 2017 Apr 01.
[Is] ISSN:1943-7722
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Objectives: GATA binding factor 1 (GATA1) is a transcription factor essential for erythromegakaryocytic differentiation. Given its function in lineage specification, we sought to evaluate the immunohistochemical profile of GATA1 in normal marrow and acute leukemia and assess the use of GATA1 as a specific erythromegakaryocytic immunohistochemical marker. Methods: Immunohistochemical studies for GATA1 expression were performed on bone marrow biopsy specimens to define its role in the evaluation of acute leukemia and other hematologic disorders. Results: In normal marrows, intense nuclear reactivity is seen in immature erythroid precursors and megakaryocytes. Weak to moderate nuclear positivity is seen in eosinophils and mast cells. In marrows involved by acute leukemia, blasts of pure erythroleukemia and acute megakaryoblastic leukemia exhibit intense nuclear GATA1 positivity, while blasts of acute myeloid leukemia of other categories are negative. GATA1 is also absent in the blasts of acute lymphoblastic leukemia/lymphoma and in the neoplastic cells of metastatic carcinoma and plasma cell neoplasms. Conclusions: Intense GATA1 nuclear expression is a sensitive and specific marker for cells of erythroid and megakaryocytic lineages and is an excellent marker for neoplastic cells of pure erythroleukemia and acute megakaryoblastic leukemia.
[Mh] Termos MeSH primário: Fator de Transcrição GATA1/metabolismo
Leucemia Eritroblástica Aguda/metabolismo
Leucemia Megacarioblástica Aguda/metabolismo
[Mh] Termos MeSH secundário: Medula Óssea/metabolismo
Medula Óssea/patologia
Diferenciação Celular
Núcleo Celular/metabolismo
Células Eritroides/metabolismo
Células Eritroides/patologia
Fator de Transcrição GATA1/genética
Marcadores Genéticos/genética
Seres Humanos
Leucemia Eritroblástica Aguda/diagnóstico
Leucemia Eritroblástica Aguda/patologia
Leucemia Megacarioblástica Aguda/diagnóstico
Leucemia Megacarioblástica Aguda/patologia
Megacariócitos/metabolismo
Megacariócitos/patologia
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GATA1 Transcription Factor); 0 (GATA1 protein, human); 0 (Genetic Markers)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE
[do] DOI:10.1093/ajcp/aqx018


  10 / 5574 MEDLINE  
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[PMID]:28216155
[Au] Autor:Fujiwara T; Sasaki K; Saito K; Hatta S; Ichikawa S; Kobayashi M; Okitsu Y; Fukuhara N; Onishi Y; Harigae H
[Ad] Endereço:Department of Hematology and Rheumatology, Tohoku University Graduate School, Sendai, 2-1 Seiryo-cho, Aoba-ku, Sendai 980-8575, Japan. Electronic address: fujiwara-to@apple.email.ne.jp.
[Ti] Título:Forced FOG1 expression in erythroleukemia cells: Induction of erythroid genes and repression of myelo-lymphoid transcription factor PU.1.
[So] Source:Biochem Biophys Res Commun;485(2):380-387, 2017 Apr 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The transcription factor GATA-1-interacting protein Friend of GATA-1 (FOG1) is essential for proper transcriptional activation and repression of GATA-1 target genes; yet, the mechanisms by which FOG1 exerts its activating and repressing functions remain unknown. Forced FOG1 expression in human K562 erythroleukemia cells induced the expression of erythroid genes (SLC4A1, globins) but repressed that of GATA-2 and PU.1. A quantitative chromatin immunoprecipitation (ChIP) analysis demonstrated increased GATA-1 chromatin occupancy at both FOG1-activated as well as FOG1-repressed gene loci. However, while TAL1 chromatin occupancy was significantly increased at FOG1-activated gene loci, it was significantly decreased at FOG1-repressed gene loci. When FOG1 was overexpressed in TAL1-knocked down K562 cells, FOG1-mediated activation of HBA, HBG, and SLC4A1 was significantly compromised by TAL1 knockdown, suggesting that FOG1 may require TAL1 to activate GATA-1 target genes. Promoter analysis and quantitative ChIP analysis demonstrated that FOG1-mediated transcriptional repression of PU.1 would be mediated through a GATA-binding element located at its promoter, accompanied by significantly decreased H3 acetylation at lysine 4 and 9 (K4 and K9) as well as H3K4 trimethylation. Our results provide important mechanistic insight into the role of FOG1 in the regulation of GATA-1-regulated genes and suggest that FOG1 has an important role in inducing cells to differentiate toward the erythroid lineage rather than the myelo-lymphoid one by repressing the expression of PU.1.
[Mh] Termos MeSH primário: Proteína 1 de Troca de Ânion do Eritrócito/genética
Regulação Leucêmica da Expressão Gênica
Proteínas Nucleares/genética
Proteínas Proto-Oncogênicas/genética
Transativadores/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Acetilação
Proteína 1 de Troca de Ânion do Eritrócito/metabolismo
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Western Blotting
Linhagem Celular
Cromatina/genética
Cromatina/metabolismo
Fator de Transcrição GATA1/genética
Fator de Transcrição GATA1/metabolismo
Histonas/metabolismo
Seres Humanos
Células K562
Leucemia Eritroblástica Aguda/genética
Leucemia Eritroblástica Aguda/metabolismo
Leucemia Eritroblástica Aguda/patologia
Lisina/metabolismo
Proteínas Nucleares/metabolismo
Regiões Promotoras Genéticas/genética
Ligação Proteica
Proteínas Proto-Oncogênicas/metabolismo
Interferência de RNA
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Proteína 1 de Leucemia Linfocítica Aguda de Células T
Transativadores/metabolismo
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anion Exchange Protein 1, Erythrocyte); 0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Chromatin); 0 (GATA1 Transcription Factor); 0 (GATA1 protein, human); 0 (Histones); 0 (Nuclear Proteins); 0 (Proto-Oncogene Proteins); 0 (SLC4A1 protein, human); 0 (T-Cell Acute Lymphocytic Leukemia Protein 1); 0 (Trans-Activators); 0 (Transcription Factors); 0 (ZFPM1 protein, human); 0 (proto-oncogene protein Spi-1); 135471-20-4 (TAL1 protein, human); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170221
[St] Status:MEDLINE



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