Base de dados : MEDLINE
Pesquisa : C04.557.337.539.275 [Categoria DeCS]
Referências encontradas : 33906 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 3391 ir para página                         

  1 / 33906 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29377903
[Au] Autor:Koldehoff M; Lindemann M; Ross SR; Elmaagacli AH
[Ad] Endereço:Department of Bone Marrow Transplantation, West German Cancer Center, University Hospital of Essen, Essen, Germany.
[Ti] Título:Cytomegalovirus induces HLA-class-II-restricted alloreactivity in an acute myeloid leukemia cell line.
[So] Source:PLoS One;13(1):e0191482, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cytomegalovirus (HCMV) reactivation is found frequently after allogeneic hematopoietic stem cell transplantation (alloSCT) and is associated with an increased treatment-related mortality. Recent reports suggest a link between HCMV and a reduced risk of cancer progression in patients with acute leukemia or lymphoma after alloSCT. Here we show that HCMV can inhibit the proliferation of the acute myeloid leukemia cell line Kasumi-1 and the promyeloid leukemia cell line NB4. HCMV induced a significant up-regulation of HLA-class-II-molecules, especially HLA-DR expression and an increase of apoptosis, granzyme B, perforin and IFN-γ secretion in Kasumi-1 cells cocultured with peripheral blood mononuclear cells (PBMCs). Indolamin-2,3-dioxygenase on the other hand led only to a significant dose-dependent effect on IFN-γ secretion without effects on proliferation. The addition of CpG-rich oligonucleotides and ganciclovir reversed those antiproliferative effects. We conclude that HCMV can enhance alloreactivity of PBMCs against Kasumi-1 and NB4 cells in vitro. To determine if this phenomenon may be clinically relevant further investigations will be required.
[Mh] Termos MeSH primário: Antígenos de Histocompatibilidade Classe II/imunologia
Leucemia Mieloide Aguda/imunologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Técnicas de Cocultura
Seres Humanos
Leucemia Mieloide Aguda/terapia
Leucemia Mieloide Aguda/virologia
Transplante de Células-Tronco
Transplante Homólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Histocompatibility Antigens Class II)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180130
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191482


  2 / 33906 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29288428
[Au] Autor:Scappaticci GB; Marini BL; Nachar VR; Uebel JR; Vulaj V; Crouch A; Bixby DL; Talpaz M; Perissinotti AJ
[Ad] Endereço:Department of Pharmacy Services and Clinical Sciences, Michigan Medicine and University of Michigan College of Pharmacy, 1500 East Medical Center Drive, Ann Arbor, MI, 48109, USA.
[Ti] Título:Outcomes of previously untreated elderly patients with AML: a propensity score-matched comparison of clofarabine vs. FLAG.
[So] Source:Ann Hematol;97(4):573-584, 2018 Apr.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The 5-year overall survival (OS) in patients ≥ 60 years old with acute myeloid leukemia (AML) remains < 10%. Clofarabine-based induction (CLO) provides an alternative to low-intensity therapy (LIT) and palliative care for this population, but supporting data are conflicted. Recently, our institution adopted the FLAG regimen (fludarabine, cytarabine, and granulocyte colony-stimulating factor) based on data reporting similar outcomes to CLO in elderly patients with AML unable to tolerate anthracycline-based induction. We retrospectively analyzed the efficacy and safety of patients ≥ 60 years old with AML treated with FLAG or CLO over the past 10 years. We performed a propensity score match that provided 32 patients in each group. Patients treated with FLAG had a higher CR/CRi rate (65.6 vs. 37.5%, P = 0.045) and OS (7.9 vs. 2.8 months, P = 0.085) compared to CLO. Furthermore, FLAG was better tolerated with significantly less grade 3/4 toxicities and a shorter duration of neutropenia (18.5 vs. 30 days, P = 0.002). Finally, we performed a cost analysis that estimated savings to be $30,000-45,000 per induction with FLAG. Our study supports the use of FLAG both financially and as an effective, well-tolerated high-dose treatment regimen for elderly patients with AML. No cases of cerebellar neurotoxicity occurred.
[Mh] Termos MeSH primário: Nucleotídeos de Adenina/uso terapêutico
Envelhecimento
Antimetabólitos Antineoplásicos/uso terapêutico
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Arabinonucleosídeos/uso terapêutico
Quimioterapia de Indução
Leucemia Mieloide Aguda/tratamento farmacológico
Vidarabina/análogos & derivados
[Mh] Termos MeSH secundário: Nucleotídeos de Adenina/efeitos adversos
Nucleotídeos de Adenina/economia
Idoso
Idoso de 80 Anos ou mais
Antimetabólitos Antineoplásicos/efeitos adversos
Antimetabólitos Antineoplásicos/economia
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Protocolos de Quimioterapia Combinada Antineoplásica/economia
Arabinonucleosídeos/efeitos adversos
Arabinonucleosídeos/economia
Estudos de Casos e Controles
Doença Hepática Induzida por Substâncias e Drogas/economia
Doença Hepática Induzida por Substâncias e Drogas/epidemiologia
Doença Hepática Induzida por Substâncias e Drogas/mortalidade
Doença Hepática Induzida por Substâncias e Drogas/terapia
Estudos de Coortes
Terapia Combinada/economia
Redução de Custos
Custos e Análise de Custo
Citarabina/efeitos adversos
Citarabina/economia
Citarabina/uso terapêutico
Fator Estimulador de Colônias de Granulócitos/efeitos adversos
Fator Estimulador de Colônias de Granulócitos/economia
Fator Estimulador de Colônias de Granulócitos/uso terapêutico
Custos Hospitalares
Seres Humanos
Incidência
Quimioterapia de Indução/efeitos adversos
Quimioterapia de Indução/economia
Tempo de Internação
Leucemia Mieloide Aguda/economia
Leucemia Mieloide Aguda/mortalidade
Michigan/epidemiologia
Meia-Idade
Neutropenia/induzido quimicamente
Neutropenia/economia
Neutropenia/mortalidade
Neutropenia/terapia
Pontuação de Propensão
Estudos Retrospectivos
Análise de Sobrevida
Centros de Atenção Terciária
Vidarabina/efeitos adversos
Vidarabina/economia
Vidarabina/uso terapêutico
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adenine Nucleotides); 0 (Antimetabolites, Antineoplastic); 0 (Arabinonucleosides); 04079A1RDZ (Cytarabine); 143011-72-7 (Granulocyte Colony-Stimulating Factor); 762RDY0Y2H (clofarabine); FA2DM6879K (Vidarabine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171231
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3217-1


  3 / 33906 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29191878
[Au] Autor:Klaeger S; Heinzlmeir S; Wilhelm M; Polzer H; Vick B; Koenig PA; Reinecke M; Ruprecht B; Petzoldt S; Meng C; Zecha J; Reiter K; Qiao H; Helm D; Koch H; Schoof M; Canevari G; Casale E; Depaolini SR; Feuchtinger A; Wu Z; Schmidt T; Rueckert L; Becker W; Huenges J; Garz AK; Gohlke BO; Zolg DP; Kayser G; Vooder T; Preissner R; Hahne H; Tõnisson N; Kramer K; Götze K; Bassermann F; Schlegl J; Ehrlich HC; Aiche S; Walch A; Greif PA; Schneider S; Felder ER; Ruland J; Médard G; Jeremias I; Spiekermann K; Kuster B
[Ad] Endereço:Chair of Proteomics and Bioanalytics, Technical University of Munich (TUM), Freising, Germany.
[Ti] Título:The target landscape of clinical kinase drugs.
[So] Source:Science;358(6367), 2017 12 01.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kinase inhibitors are important cancer therapeutics. Polypharmacology is commonly observed, requiring thorough target deconvolution to understand drug mechanism of action. Using chemical proteomics, we analyzed the target spectrum of 243 clinically evaluated kinase drugs. The data revealed previously unknown targets for established drugs, offered a perspective on the "druggable" kinome, highlighted (non)kinase off-targets, and suggested potential therapeutic applications. Integration of phosphoproteomic data refined drug-affected pathways, identified response markers, and strengthened rationale for combination treatments. We exemplify translational value by discovering SIK2 (salt-inducible kinase 2) inhibitors that modulate cytokine production in primary cells, by identifying drugs against the lung cancer survival marker MELK (maternal embryonic leucine zipper kinase), and by repurposing cabozantinib to treat FLT3-ITD-positive acute myeloid leukemia. This resource, available via the ProteomicsDB database, should facilitate basic, clinical, and drug discovery research and aid clinical decision-making.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Descoberta de Drogas/métodos
Terapia de Alvo Molecular
Inibidores de Proteínas Quinases/farmacologia
Proteômica/métodos
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/química
Linhagem Celular Tumoral
Citocinas/metabolismo
Seres Humanos
Leucemia Mieloide Aguda/tratamento farmacológico
Leucemia Mieloide Aguda/enzimologia
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/enzimologia
Camundongos
Inibidores de Proteínas Quinases/química
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Ensaios Antitumorais Modelo de Xenoenxerto
Tirosina Quinase 3 Semelhante a fms/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Cytokines); 0 (Protein Kinase Inhibitors); EC 2.7.1.- (MELK protein, human); EC 2.7.1.- (salt-inducible kinase-2, human); EC 2.7.10.1 (FLT3 protein, human); EC 2.7.10.1 (fms-Like Tyrosine Kinase 3); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE


  4 / 33906 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29286055
[Au] Autor:Garcia JS; Percival ME
[Ad] Endereço:Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA. jacqueline_garcia@dfci.harvard.edu.
[Ti] Título:Midostaurin for the treatment of adult patients with newly diagnosed acute myeloid leukemia that is FLT3 mutation-positive.
[So] Source:Drugs Today (Barc);53(10):531-543, 2017 Oct.
[Is] ISSN:1699-3993
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:Midostaurin is a multitargeted tyrosine kinase inhibitor (TKI) that potently inhibits activated fms-related tyrosine kinase 3 (FLT3) in the nanomolar range and other kinases including platelet-derived growth factor receptors α (PDGFR- α) and ß (PDGFR- ß), cyclin-dependent kinase, proto-oncogene tyrosine-protein kinase Src, tyrosine-protein kinase Fgr, spleen tyrosine kinase (Syk), KIT proto-oncogene receptor tyrosine kinase and the major vascular endothelial growth factor receptor (VEGFR). Activating mutations in FLT3, which is one of the more common acute myeloid leukemia (AML) mutations, particularly those that result in an FLT3-ITD (internal tandem duplication) mutation, confer poor prognosis and represent a therapeutic target. Small molecule TKIs that vary in potency and selectivity for FLT3 are under investigation. Here, we provide a comprehensive review of the preclinical and clinical activity of midostaurin, a recently approved drug indicated to be used in combination with cytarabine and daunorubicin induction and cytarabine consolidation chemotherapy for the treatment of AML featuring an FLT3 mutation.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Leucemia Mieloide Aguda/tratamento farmacológico
Mutação
Inibidores de Proteínas Quinases/uso terapêutico
Estaurosporina/análogos & derivados
Tirosina Quinase 3 Semelhante a fms/antagonistas & inibidores
Tirosina Quinase 3 Semelhante a fms/genética
[Mh] Termos MeSH secundário: Adulto
Ensaios Clínicos como Assunto
Interações Medicamentosas
Seres Humanos
Leucemia Mieloide Aguda/genética
Estaurosporina/efeitos adversos
Estaurosporina/farmacocinética
Estaurosporina/farmacologia
Estaurosporina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Protein Kinase Inhibitors); EC 2.7.10.1 (FLT3 protein, human); EC 2.7.10.1 (fms-Like Tyrosine Kinase 3); H88EPA0A3N (Staurosporine); ID912S5VON (midostaurin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171230
[St] Status:MEDLINE
[do] DOI:10.1358/dot.2017.53.10.2717625


  5 / 33906 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29298978
[Au] Autor:Lee SI; Celik S; Logsdon BA; Lundberg SM; Martins TJ; Oehler VG; Estey EH; Miller CP; Chien S; Dai J; Saxena A; Blau CA; Becker PS
[Ad] Endereço:Paul G. Allen School of Computer Science and Engineering, University of Washington, 185 E Stevens Way NE, Seattle, WA, 98195, USA. suinlee@cs.washington.edu.
[Ti] Título:A machine learning approach to integrate big data for precision medicine in acute myeloid leukemia.
[So] Source:Nat Commun;9(1):42, 2018 01 03.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cancers that appear pathologically similar often respond differently to the same drug regimens. Methods to better match patients to drugs are in high demand. We demonstrate a promising approach to identify robust molecular markers for targeted treatment of acute myeloid leukemia (AML) by introducing: data from 30 AML patients including genome-wide gene expression profiles and in vitro sensitivity to 160 chemotherapy drugs, a computational method to identify reliable gene expression markers for drug sensitivity by incorporating multi-omic prior information relevant to each gene's potential to drive cancer. We show that our method outperforms several state-of-the-art approaches in identifying molecular markers replicated in validation data and predicting drug sensitivity accurately. Finally, we identify SMARCA4 as a marker and driver of sensitivity to topoisomerase II inhibitors, mitoxantrone, and etoposide, in AML by showing that cell lines transduced to have high SMARCA4 expression reveal dramatically increased sensitivity to these agents.
[Mh] Termos MeSH primário: DNA Helicases/genética
Resistência a Medicamentos Antineoplásicos/genética
Leucemia Mieloide Aguda/genética
Aprendizado de Máquina
Proteínas Nucleares/genética
Medicina de Precisão/métodos
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Algoritmos
Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
Biomarcadores Tumorais/metabolismo
Linhagem Celular
Conjuntos de Dados como Assunto
Etoposídeo/farmacologia
Etoposídeo/uso terapêutico
Seres Humanos
Leucemia Mieloide Aguda/tratamento farmacológico
Inibidores da Topoisomerase II/farmacologia
Inibidores da Topoisomerase II/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Biomarkers, Tumor); 0 (Nuclear Proteins); 0 (Topoisomerase II Inhibitors); 0 (Transcription Factors); 6PLQ3CP4P3 (Etoposide); EC 3.6.1.- (SMARCA4 protein, human); EC 3.6.4.- (DNA Helicases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180105
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02465-5


  6 / 33906 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29200853
[Au] Autor:Briot T; Roger E; Lautram N; Verger A; Clavreul A; Lagarce F
[Ad] Endereço:Micro & Nanomédecines Translationelles - MINT, UNIV Angers, INSERM 1066, CNRS 6021, Université Bretagne Loire, MINT IBS-CHU.
[Ti] Título:Development and in vitro evaluations of new decitabine nanocarriers for the treatment of acute myeloid leukemia.
[So] Source:Int J Nanomedicine;12:8427-8442, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Decitabine is a hydrophilic drug that acts by hypomethylating DNA. Decitabine is used in Europe for the treatment of acute myeloid leukemia (AML) in patients aged ≥65 years. However, it can only be administered intravenously due to very low oral bioavailability and a large distribution volume. Oral administration would allow outpatient treatment, improving quality of life and reducing treatment costs. The present study proposes to develop lipid nanocapsules (LNCs), originally designed for lipophilic drugs, to encapsulate decitabine. Two different formulations of LNCs were designed: LNCs based on a high proportion of Transcutol HP (THP-LNCs) and LNCs associated with a mixture of Transcutol HP and Tween 80 (THP-T80-LNCs). The second formulation had a diameter of 26.5±0.5 nm, high encapsulation efficiency (>85%), and a drug payload of 472±64 µg/mL. Decitabine-loaded THP-T80-LNC cytotoxicity was evaluated on two AML cell lines depending on their decitabine resistance: HEL (not resistant) and HL-60 (resistant). The permeability of decitabine-loaded THP-T80-LNCs was also evaluated on Caco-2 cell monolayers. Decitabine cytotoxicity against HEL and HL-60 was higher when decitabine was loaded in THP-T80-LNCs than when free. Apparent permeability on Caco-2 cell monolayers was also increased, suggesting a potentially useful formulation to increase the oral bioavailability of decitabine.
[Mh] Termos MeSH primário: Azacitidina/análogos & derivados
Portadores de Fármacos/química
Leucemia Mieloide Aguda/tratamento farmacológico
Nanocápsulas/administração & dosagem
[Mh] Termos MeSH secundário: Administração Oral
Antimetabólitos Antineoplásicos/administração & dosagem
Antimetabólitos Antineoplásicos/farmacocinética
Azacitidina/administração & dosagem
Azacitidina/farmacocinética
Disponibilidade Biológica
Células CACO-2
Linhagem Celular Tumoral
Portadores de Fármacos/administração & dosagem
Liberação Controlada de Fármacos
Resistência a Medicamentos Antineoplásicos/efeitos dos fármacos
Estabilidade de Medicamentos
Etilenoglicóis/química
Seres Humanos
Lipídeos/química
Nanocápsulas/química
Polissorbatos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 0 (Drug Carriers); 0 (Ethylene Glycols); 0 (Lipids); 0 (Nanocapsules); 0 (Polysorbates); 776B62CQ27 (decitabine); A1A1I8X02B (carbitol); M801H13NRU (Azacitidine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S147659


  7 / 33906 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28460451
[Au] Autor:Tsitsipatis D; Jayavelu AK; Müller JP; Bauer R; Schmidt-Arras D; Mahboobi S; Schnöder TM; Heidel F; Böhmer FD
[Ad] Endereço:Institute of Molecular Cell Biology, CMB, Jena University Hospital, Jena, Germany.
[Ti] Título:Synergistic killing of FLT3ITD-positive AML cells by combined inhibition of tyrosine-kinase activity and N-glycosylation.
[So] Source:Oncotarget;8(16):26613-26624, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fms-like tyrosine kinase 3 (FLT3) with internal tandem duplications (ITD) is a major oncoprotein in acute myeloid leukemia (AML), and confers an unfavorable prognosis. Interference with FLT3ITD signaling is therefore pursued as a promising therapeutic strategy. In this study we show that abrogation of FLT3ITD glycoprotein maturation using low doses of the N-glycosylation inhibitor tunicamycin has anti-proliferative and pro-apoptotic effects on FLT3ITD-expressing human and murine cell lines. This effect is mediated in part by arresting FLT3ITD in an underglycosylated state and thereby attenuating FLT3ITD-driven AKT and ERK signaling. In addition, tunicamycin caused pronounced endoplasmatic reticulum stress and apoptosis through activation of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and activation of the gene encoding CCAAT-enhancer-binding protein homologous protein (CHOP). PERK inhibition with a small molecule attenuated CHOP induction and partially rescued cells from apoptosis. Combination of tunicamycin with potent FLT3ITD kinase inhibitors caused synergistic cell killing, which was highly selective for cell lines and primary AML cells expressing FLT3ITD. Although tunicamycin is currently not a clinically applicable drug, we propose that mild inhibition of N-glycosylation may have therapeutic potential in combination with FLT3 kinase inhibitors for FLT3ITD-positive AML.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Duplicação Gênica
Leucemia Mieloide Aguda/genética
Inibidores de Proteínas Quinases/farmacologia
Sequências de Repetição em Tandem
Tirosina Quinase 3 Semelhante a fms/genética
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Apoptose/genética
Linhagem Celular Tumoral
Sinergismo Farmacológico
Estresse do Retículo Endoplasmático
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Expressão Gênica
Glicosilação/efeitos dos fármacos
Seres Humanos
Leucemia Mieloide Aguda/tratamento farmacológico
Leucemia Mieloide Aguda/metabolismo
Leucemia Mieloide Aguda/patologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Células Tumorais Cultivadas
Tunicamicina/farmacologia
Tirosina Quinase 3 Semelhante a fms/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Protein Kinase Inhibitors); 11089-65-9 (Tunicamycin); EC 2.7.10.1 (fms-Like Tyrosine Kinase 3); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15772


  8 / 33906 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29390324
[Au] Autor:Harada Y; Nishiwaki S; Sugimoto T; Onodera K; Goto T; Sato T; Kamoshita S; Kawashima N; Seto A; Okuno S; Yamamoto S; Iwasaki T; Ozawa Y; Miyamura K; Akatsuka Y; Sugiura I
[Ad] Endereço:Division of Hematology and Oncology, Toyohashi Municipal Hospital.
[Ti] Título:Successful treatment with allogeneic stem cell transplantation followed by DLI and TKIs for e6a2 BCR-ABL-positive acute myeloid leukaemia: A case report and literature review.
[So] Source:Medicine (Baltimore);96(50):e9160, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Patients with the e6a2 BCR-ABL transcript, 1 of the atypical transcripts, have been reported to have a poor prognosis, and allogeneic stem cell transplantation (ASCT) can be considered as additional therapy. However, long-term survival after ASCT for this disease is rare. PATIENT CONCERNS: This report concerns a 55-year-old female patient with e6a2 BCR-ABL-positive acute myeloid leukemia including the outcome of ASCT followed by donor lymphocyte infusion (DLI). DIAGNOSES: The breakpoint was confirmed by direct sequencing. Her minimal residual disease could be detected by nested reverse-transcription polymerase chain reaction using primers for the minor BCR-ABL (e1a2) transcript. INTERVENTIONS: Treatment with tyrosine kinase inhibitors (TKIs) and ASCT followed by DLI. OUTCOMES: Despite multiple cytogenetic and molecular relapses after ASCT, she remains in molecular remission at 46 months after ASCT. LESSONS: This case indicates the efficacy of the combination of the graft-versus-leukemia effect and TKIs for e6a2 BCR-ABL-positive acute leukemia. When the Philadelphia chromosome with an unusual chromosomal breakpoint is suggested, we should clarify the breakpoint because that information can aid molecular assessments and decisions to provide an additional or alternative therapy.
[Mh] Termos MeSH primário: Transplante de Células-Tronco Hematopoéticas
Leucemia Mieloide Aguda/terapia
[Mh] Termos MeSH secundário: Feminino
Proteínas de Fusão bcr-abl
Efeito Enxerto vs Leucemia
Seres Humanos
Transfusão de Linfócitos
Meia-Idade
Neoplasia Residual
Cromossomo Filadélfia
Proteínas Tirosina Quinases/antagonistas & inibidores
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.2 (Fusion Proteins, bcr-abl)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009160


  9 / 33906 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27771959
[Au] Autor:Khan M; Mansoor AE; Kadia TM
[Ad] Endereço:Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
[Ti] Título:Future prospects of therapeutic clinical trials in acute myeloid leukemia.
[So] Source:Future Oncol;13(6):523-535, 2017 Mar.
[Is] ISSN:1744-8301
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Acute myeloid leukemia (AML) is a markedly heterogeneous hematological malignancy that is most commonly seen in elderly adults. The response to current therapies to AML is quite variable, and very few new drugs have been recently approved for use in AML. This review aims to discuss the issues with current trial design for AML therapies, including trial end points, patient enrollment, cost of drug discovery and patient heterogeneity. We also discuss the future directions in AML therapeutics, including intensification of conventional therapy and new drug delivery mechanisms; targeted agents, including epigenetic therapies, cell cycle regulators, hypomethylating agents and chimeric antigen receptor T-cell therapy; and detail of the possible agents that may be incorporated into the treatment of AML in the future.
[Mh] Termos MeSH primário: Leucemia Mieloide Aguda/terapia
[Mh] Termos MeSH secundário: Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Biomarcadores
Ensaios Clínicos como Assunto
Custos de Medicamentos
Seres Humanos
Leucemia Mieloide Aguda/diagnóstico
Leucemia Mieloide Aguda/mortalidade
Projetos de Pesquisa
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.2217/fon-2016-0262


  10 / 33906 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
[PMID]:28746590
[Au] Autor:Campregher PV; Mattos VRP; Salvino MA; Santos FPS; Hamerschlak N
[Ad] Endereço:Hospital Israelita Albert Einstein, São Paulo, SP, Brazil.
[Ti] Título:Successful treatment of post-transplant relapsed acute myeloid leukemia with FLT3 internal tandem duplication using the combination of induction chemotherapy, donor lymphocyte infusion, sorafenib and azacitidine. Report of three cases.
[So] Source:Einstein (Sao Paulo);15(3):355-358, 2017 Jul-Sep.
[Is] ISSN:2317-6385
[Cp] País de publicação:Brazil
[La] Idioma:eng; por
[Ab] Resumo:Acute myeloid leukemia is a hematopoietic stem cell neoplastic disease associated with high morbidity and mortality. The presence of FLT3 internal tandem duplication mutations leads to high rates of relapse and decreased overall survival. Patients with FLT3 internal tandem duplication are normally treated with hematopoietic stem cell transplantation in first complete remission. Nevertheless, the incidence of post-transplant relapse is considerable in this group of patients, and the management of this clinical condition is challenging. The report describes the outcomes of patients with FLT3 internal tandem duplication positive acute myeloid leukemia who relapsed after allogeneic hematopoietic stem cell transplantation and were treated with the combination of re-induction chemotherapy, donor lymphocyte infusion, sorafenib and azacitidine. Three cases are described and all patients achieved prolonged complete remission with the combined therapy. The combination of induction chemotherapy followed by donor lymphocyte infusion, and the maintenance with azacitidine and sorafenib can be effective approaches in the treatment of post-hematopoietic stem cell transplant and relapsed FLT3 internal tandem duplication positive acute myeloid leukemia patients. This strategy should be further explored in the context of clinical trials.
[Mh] Termos MeSH primário: Antineoplásicos/administração & dosagem
Azacitidina/administração & dosagem
Quimioterapia de Indução
Leucemia Mieloide Aguda/terapia
Transfusão de Linfócitos
Niacinamida/análogos & derivados
Compostos de Fenilureia/administração & dosagem
Tirosina Quinase 3 Semelhante a fms/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Terapia Combinada/métodos
Feminino
Seres Humanos
Leucemia Mieloide Aguda/genética
Masculino
Meia-Idade
Recidiva Local de Neoplasia/terapia
Niacinamida/administração & dosagem
Recidiva
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Phenylurea Compounds); 25X51I8RD4 (Niacinamide); 9ZOQ3TZI87 (sorafenib); EC 2.7.10.1 (FLT3 protein, human); EC 2.7.10.1 (fms-Like Tyrosine Kinase 3); M801H13NRU (Azacitidine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE



página 1 de 3391 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde