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[PMID]:29185091
[Au] Autor:Kolben T; Jeschke U; Reimer T; Karsten N; Schmoeckel E; Semmlinger A; Mahner S; Harbeck N; Kolben TM
[Ad] Endereço:Department of Obstetrics and Gynecology, University Hospital, Ludwig-Maximilians-University Munich, Marchioninistr. 15, 81377, Munich, Germany. Thomas.Kolben@med.uni-muenchen.de.
[Ti] Título:Induction of apoptosis in breast cancer cells in vitro by Fas ligand reverse signaling.
[So] Source:J Cancer Res Clin Oncol;144(2):249-256, 2018 Feb.
[Is] ISSN:1432-1335
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: The Fas-antigen is a cell surface receptor that transduces apoptotic signals into cells. The purpose of this study was to evaluate FasL expression in breast cancer and to elucidate the role of its signaling in different breast cancer cell lines. METHODS: T47D and MCF7 cells were used and cultured in Dulbecco's modified Eagle's medium. FasL translocation to the membrane was achieved by culturing the cells in the presence of human interferon-γ (IFNγ). Translocation was detected by immunofluorescence. The ability of a Fas:Fc fusion protein to trigger apoptosis in these cells was investigated by cell death detection ELISA. After incubation with IFNγ for 4 h and 18 h, apoptosis was assessed in response to treatment with Fas:Fc. RESULTS: Immunofluorescence revealed that the used cell lines were positive for FasL which was increased and changed to more membrane-bound FasL expression after IFNγ stimulation. After stimulation with 50 IU/ml IFNγ, Fas:Fc significantly increased MCF7 apoptosis (1.39 ± 0.06-fold, p = 0.0004) after 18 h. After stimulation with 100 IU/ml, Fas:Fc significantly increased apoptosis both after 4 h (1.49 ± 0.15-fold, p = 0.018) and 18 h (1.30 ± 0.06-fold, p = 0.013). In T47D cells this effect was seen after 4 h of stimulation with 50 IU/ml and addition of Fas:Fc (1.6 ± 0.08-fold, p = 0.03). CONCLUSION: Membrane-bound FasL expression could be induced by IFNγ in a breast cancer cell model. More importantly, in the presence of IFNγ the Fas:Fc fusion protein was able to transmit pro-apoptotic signals to T47D and MCF7 cells, significantly inducing apoptosis. The current findings support further in vivo studies regarding FasL activation as a potential target for therapeutic intervention in breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Proteína Ligante Fas/metabolismo
[Mh] Termos MeSH secundário: Apoptose/efeitos dos fármacos
Apoptose/fisiologia
Neoplasias da Mama/tratamento farmacológico
Ensaio de Imunoadsorção Enzimática
Proteína Ligante Fas/genética
Feminino
Imunofluorescência
Seres Humanos
Fragmentos Fc das Imunoglobulinas/genética
Interferon gama/farmacologia
Células MCF-7
Proteínas Recombinantes de Fusão/genética
Proteínas Recombinantes de Fusão/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FASLG protein, human); 0 (Fas Ligand Protein); 0 (IFNG protein, human); 0 (Immunoglobulin Fc Fragments); 0 (Recombinant Fusion Proteins); 82115-62-6 (Interferon-gamma)
[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:171130
[St] Status:MEDLINE
[do] DOI:10.1007/s00432-017-2551-y


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[PMID]:29419701
[Au] Autor:Zhang DF; Jiang GB; Qin CQ; Liu DX; Hu YJ; Zhou J; Niu YM
[Ad] Endereço:Center for Evidence-Based Medicine and Clinical Research, Department of Endocrine Vascular Surgery, Taihe Hospital, Shiyan.
[Ti] Título:Quantitative assessment of the relationship between Fas/FasL genes polymorphisms and head and neck cancer risk.
[So] Source:Medicine (Baltimore);97(6):e9873, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Molecular epidemiological studies have demonstrated a closer association between Fas/FasL polymorphisms and head and neck cancer (HNC) risk, and the results of these published studies were inconsistent. We therefore performed this meta-analysis to explore the associations between Fas/FasL polymorphisms and HNC risk. METHODS: Four online databases (PubMed, Embase, CNKI, and Wanfang) were searched. Odds ratios (ORs) with 95% confidence interval (95% CIs) were calculated to assess the association between Fas -670A>G, Fas -1377G>A, and FasL -844C>T polymorphisms and HNC risk. In addition, heterogeneity, accumulative/sensitivity analysis, and publication bias were conducted to check the statistical power. RESULTS: Overall, 9 related publications (20 independent case-control studies) involving 3179 patients and 4217 controls were identified. Significant association of protective effects was observed between FasL -844C>T polymorphism and HNC risk in codominant and dominant model models (CT vs CC: OR = 0.89, 95% CI = 0.79-1.00, P = .05, I = 38.3%, CT+TT vs CC: OR = 0.88, 95% CI = 0.79-0.98, P = .02, I = 35.8%). Furthermore, the similar protective effects were observed the subgroup analysis of in Asian population and population-based controls group. CONCLUSION: Our meta-analysis indicated that FasL -844C>T polymorphism plays a protective role against HNC development, but the Fas -670A>G and Fas -1377G>A polymorphisms maybe not associated with HNC risk.
[Mh] Termos MeSH primário: Proteína Ligante Fas/genética
Neoplasias de Cabeça e Pescoço/genética
[Mh] Termos MeSH secundário: Grupo com Ancestrais do Continente Asiático/genética
Seres Humanos
Polimorfismo de Nucleotídeo Único
Fatores de Proteção
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (FASLG protein, human); 0 (Fas Ligand Protein)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009873


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[PMID]:28468172
[Au] Autor:Heo KW; Park SK; Lee YM; Choe SH; Gu PM; Hong TU; Hur DY
[Ad] Endereço:*Department of Otorhinolaryngology-Head and Neck Surgery †Department of Anatomy and Research Center for Tumor Immunology, Inje University Busan Paik Hospital, Busan, South Korea.
[Ti] Título:Methotrexate Induces Apoptosis in Organ-Cultured Nasal Polyps Via the Fas Pathway.
[So] Source:J Craniofac Surg;28(3):806-809, 2017 May.
[Is] ISSN:1536-3732
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Methotrexate (MTX) is very effective when used to treat chronic inflammatory diseases, and also induces apoptosis in nasal polyps (NPs). Increasing evidence suggests that Fas-Fas ligand (FasL) interactions activate multiple pathways involved in the regulation of immune and inflammatory cell functions. The aim of the present study was to identify pathways activated by Fas signaling when NPs were treated with MTX. METHODS: Nasal polyps tissues were cultured using an air-liquid interface organ culture method. Cultures were maintained in the absence or presence of MTX (10 or 100 µM) for 24 hours. The authors used the reverse transcription-polymerase chain reaction method and Western blotting to identify pathways activated by Fas when NPs were treated with MTX. RESULTS: The Fas mRNA expression ratio was unchanged upon MTX treatment, but the FasL mRNA expression ratio was significantly higher in MTX-treated than nontreated polyps. In addition, the expression levels of the Fas and FasL proteins were significantly higher in polyps treated with both 10 and 100 µM MTX compared with nontreated polyps. CONCLUSIONS: Methotrexate induces apoptosis in NPs via the Fas pathway. Future studies should explore the topical use of MTX for NP control. Methotrexate may be a useful alternative steroid-sparing agent for the treatment of NPs.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Proteína Ligante Fas/genética
Regulação da Expressão Gênica
Metotrexato/farmacologia
Pólipos Nasais/patologia
Técnicas de Cultura de Órgãos/métodos
RNA Mensageiro/genética
[Mh] Termos MeSH secundário: Apoptose/genética
Western Blotting
Proteína Ligante Fas/biossíntese
Seres Humanos
Imunossupressores/uso terapêutico
Pólipos Nasais/tratamento farmacológico
Pólipos Nasais/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FASLG protein, human); 0 (Fas Ligand Protein); 0 (Immunosuppressive Agents); 0 (RNA, Messenger); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:D
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1097/SCS.0000000000003562


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[PMID]:29216642
[Au] Autor:Yang W; Huang J; Xiao B; Liu Y; Zhu Y; Wang F; Sun S
[Ti] Título:Taurine Protects Mouse Spermatocytes from Ionizing Radiation-Induced Damage Through Activation of Nrf2/HO-1 Signaling.
[So] Source:Cell Physiol Biochem;44(4):1629-1639, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: The increasing prevalence of ionizing radiation exposure has inevitably raised public concern over the potential detrimental effects of ionizing radiation on male reproductive system function. The detection of drug candidates to prevent reproductive system from damage caused by ionizing radiation is urgent. We aimed to investigate the protective role of taurine on the injury of mouse spermatocyte-derived cells (GC-2) subjected to ionizing radiation. METHODS: mouse spermatocytes (GC-2 cells) were exposed to ionizing radiation with or without treatment of Taurine. The effect of ionizing radiation and Taurine treatment on GC-2 cells were evaluated by cell viability assay (CCK8), cell cycle and apoptosis. The relative protein abundance change was determined by Western blotting. The siRNA was used to explore whether Nrf2 signaling was involved in the cytoprotection of Taurine. RESULTS: Taurine significantly inhibited the decrease of cell viability, percentage of apoptotic cells and cell cycle arrest induced by ionizing radiation. Western blot analysis showed that taurine significantly limited the ionizing radiation-induced down-regulation of CyclinB1 and CDK1, and suppressed activation of Fas/FasL system pathway. In addition, taurine treatment significantly increased the expression of Nrf2 and HO-1 in GC-2 cells exposed to ionizing radiation, two components in antioxidant pathway. The above cytoprotection of Taurine was blocked by siNrf2. CONCLUSION: Our results demonstrate that taurine has the potential to effectively protect GC-2 cells from ionizing radiation- triggered damage via upregulation of Nrf2/HO-1 signaling.
[Mh] Termos MeSH primário: Heme Oxigenase-1/metabolismo
Fator 2 Relacionado a NF-E2/metabolismo
Substâncias Protetoras/farmacologia
Radiação Ionizante
Transdução de Sinais/efeitos dos fármacos
Taurina/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Apoptose/efeitos da radiação
Proteína Quinase CDC2/metabolismo
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Pontos de Checagem do Ciclo Celular/efeitos da radiação
Linhagem Celular
Ciclina B1/metabolismo
Regulação para Baixo/efeitos dos fármacos
Proteína Ligante Fas/metabolismo
Masculino
Camundongos
Fator 2 Relacionado a NF-E2/antagonistas & inibidores
Fator 2 Relacionado a NF-E2/genética
Estresse Oxidativo/efeitos dos fármacos
Estresse Oxidativo/efeitos da radiação
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Transdução de Sinais/efeitos da radiação
Espermatócitos/citologia
Espermatócitos/efeitos dos fármacos
Espermatócitos/metabolismo
Receptor fas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclin B1); 0 (Fas Ligand Protein); 0 (Fas protein, mouse); 0 (Fasl protein, mouse); 0 (NF-E2-Related Factor 2); 0 (Protective Agents); 0 (RNA, Small Interfering); 0 (fas Receptor); 1EQV5MLY3D (Taurine); EC 1.14.14.18 (Heme Oxygenase-1); EC 2.7.11.22 (CDC2 Protein Kinase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1159/000485762


  5 / 7328 MEDLINE  
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[PMID]:29176759
[Au] Autor:Magalhães LMD; Viana A; de Jesus AC; Chiari E; Galvão L; Gomes JA; Gollob KJ; Dutra WO
[Ad] Endereço:Laboratório de Biologia das Interações Celulares, Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
[Ti] Título:Distinct Trypanosoma cruzi isolates induce activation and apoptosis of human neutrophils.
[So] Source:PLoS One;12(11):e0188083, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neutrophils are critical players in the first line of defense against pathogens and in the activation of subsequent cellular responses. We aimed to determine the effects of the interaction of Trypanosoma cruzi with human neutrophils, using isolates of the two major discrete type units (DTUs) associated with Chagas' disease in Latin America (clone Col1.7G2 and Y strain, DTU I and II, respectively). Thus, we used CFSE-stained trypomastigotes to measure neutrophil-T. cruzi interaction, neutrophil activation, cytokine expression and death, after infection with Col1.7G2 and Y strain. Our results show that the frequency of CFSE+ neutrophils, indicative of interaction, and CFSE intensity on a cell-per-cell basis were similar when comparing Col1.7G2 and Y strains. Interaction with T. cruzi increased neutrophil activation, as measured by CD282, CD284, TNF and IL-12 expression, although at different levels between the two strains. No change in IL-10 expression was observed after interaction of neutrophils with either strain. We observed that exposure to Y and Col1.7G2 caused marked neutrophil death. This was specific to neutrophils, since interaction of either strain with monocytes did not cause death. Our further analysis showed that neutrophil death was a result of apoptosis, which was associated with an upregulation of TNF-receptor, TNF and FasLigand, but not of Fas. Induction of TNF-associated neutrophil apoptosis by the different T. cruzi isolates may act as an effective common mechanism to decrease the host's immune response and favor parasite survival.
[Mh] Termos MeSH primário: Apoptose
Ativação de Neutrófilo
Neutrófilos/citologia
Trypanosoma cruzi/isolamento & purificação
[Mh] Termos MeSH secundário: Adulto
Antígenos CD/metabolismo
Sobrevivência Celular
Proteína Ligante Fas/metabolismo
Fluoresceínas/metabolismo
Seres Humanos
Interleucina-10/metabolismo
Interleucina-12/metabolismo
Neutrófilos/metabolismo
Receptores do Fator de Necrose Tumoral/metabolismo
Succinimidas/metabolismo
Receptor 2 Toll-Like/metabolismo
Receptor 4 Toll-Like/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
Adulto Jovem
Receptor fas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5-(6)-carboxyfluorescein diacetate succinimidyl ester); 0 (Antigens, CD); 0 (FAS protein, human); 0 (Fas Ligand Protein); 0 (Fluoresceins); 0 (Receptors, Tumor Necrosis Factor); 0 (Succinimides); 0 (Toll-Like Receptor 2); 0 (Toll-Like Receptor 4); 0 (Tumor Necrosis Factor-alpha); 0 (fas Receptor); 130068-27-8 (Interleukin-10); 187348-17-0 (Interleukin-12)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188083


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[PMID]:29187439
[Au] Autor:Werner JM; Kuhl S; Stavrinou P; Röhn G; Krischek B; Blau T; Goldbrunner R; Timmer M
[Ad] Endereço:Department of General Neurosurgery, Center for Neurosurgery, University Hospital Cologne, Cologne, Germany.
[Ti] Título:Expression of FAS-L Differs from Primary to Relapsed Low-grade Gliomas and Predicts Progression-free Survival.
[So] Source:Anticancer Res;37(12):6639-6648, 2017 12.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The tumor necrosis factor FAS is overexpressed in high-grade gliomas (HGG). Only little is known about FAS or FAS ligand (FAS-L) in low-grade gliomas (LGG). We explored FAS/FAS-L expression in LGG, focusing on differences in primary and relapsed LGG and on its prognostic value. PATIENTS AND METHODS: A total of 133 glioma samples (73 LGG, 60 HGG) were collected. The LGG samples included 15 matched pairs of primary and relapsed tumors. RT-PCR was performed to measure FAS/FAS-L expression, using subunit A, flavoprotein variant (SDHA) as housekeeper. Clinical data included progression free- (PFS) and overall survival (OS). RESULTS: LGG showed significantly lower FAS but higher FAS-L expression than HGG. The FAS-L expression was higher in primary compared to relapsed LGG and had a positive prognostic value concerning PFS (median 45.20 vs. 31.37 months). CONCLUSION: FAS-L could act as a prognostic marker and potential target in primary LGG.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/genética
Proteína Ligante Fas/genética
Regulação Neoplásica da Expressão Gênica
Glioma/genética
[Mh] Termos MeSH secundário: Adulto
Neoplasias Encefálicas/metabolismo
Neoplasias Encefálicas/patologia
Progressão da Doença
Proteína Ligante Fas/metabolismo
Feminino
Glioma/patologia
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Gradação de Tumores
Prognóstico
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Receptor fas/genética
Receptor fas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fas Ligand Protein); 0 (fas Receptor)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171211
[Lr] Data última revisão:
171211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE


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[PMID]:28985848
[Au] Autor:Qiu M; Chen Y; Chen L; Zeng J; Liu J
[Ad] Endereço:Department of Thoracic Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China. Electronic address: qml-817@163.com.
[Ti] Título:Transforming growth factor ß1 and Fas ligand synergistically enhance immune tolerance in dendritic cells in liver transplantation.
[So] Source:J Surg Res;218:180-193, 2017 Oct.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Long-term survival of patients following liver transplantation can be achieved by application of genetically modified, immune tolerogenic immature dendritic cells (imDCs) to overcome allograft-induced acute cellular rejection, a major cause of death. In this study, using a rat model of liver transplantation, we determined whether cotransfection of transforming growth factor ß1 (TGF-ß1) and Fas ligand (FasL) in imDCs synergistically enhances immune tolerance. MATERIALS AND METHODS: We first determined the immune tolerogenic effects of TGF-ß1 and FasL independently or together in imDCs by measuring the levels of CD86 and CD80 and by assessing T-cell proliferation using mixed lymphocyte reaction tests. Next, a rat model of liver transplantation, in which dark agouti and Lewis rats treated with DCs exogenously expressing TGF-ß1 and/or FasL served as donors and recipients, respectively, was used to examine TGF-ß1/FasL-induced immune tolerance. Specifically, we assessed the Banff rejection activity index (RAI), liver functions (alanine transaminase and total bilirubin levels), serum levels of interleukin (IL)-1, IL-10, and IL-12, apoptosis by TUNEL, and posttransplant survival. RESULTS: TGF-ß1/FasL cotransfection of imDCs resulted in greater reduction of CD85 and CD80 expression and T-cell proliferation than a monotransfection. Cotransfected imDCs also showed reduced RAI scores, decreased plasma alanine transaminase and total bilirubin, altered cytokine levels, increased apoptosis, and prolonged survival than monotransfected imDCs in liver-allografted rats. CONCLUSIONS: By enhancing immune tolerance, reducing liver damage, and achieving long-term postsurgery survival, TGF-ß1/FasL cotransfection of imDCs may prove more beneficial for patients undergoing liver transplantation.
[Mh] Termos MeSH primário: Células Dendríticas/metabolismo
Proteína Ligante Fas/genética
Rejeição de Enxerto/prevenção & controle
Tolerância Imunológica
Fator de Crescimento Transformador beta1/genética
[Mh] Termos MeSH secundário: Animais
Apoptose
Células Cultivadas
Proteína Ligante Fas/metabolismo
Técnicas de Transferência de Genes
Imunofenotipagem
Interleucinas/sangue
Fígado/patologia
Transplante de Fígado
Masculino
Ratos Endogâmicos Lew
Linfócitos T/fisiologia
Fator de Crescimento Transformador beta1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Fas Ligand Protein); 0 (Interleukins); 0 (Transforming Growth Factor beta1)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171008
[St] Status:MEDLINE


  8 / 7328 MEDLINE  
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[PMID]:28716979
[Au] Autor:Bustamante A; López-Cancio E; Pich S; Penalba A; Giralt D; García-Berrocoso T; Ferrer-Costa C; Gasull T; Hernández-Pérez M; Millan M; Rubiera M; Cardona P; Cano L; Quesada H; Terceño M; Silva Y; Castellanos M; Garces M; Reverté S; Ustrell X; Marés R; Baiges JJ; Serena J; Rubio F; Salas E; Dávalos A; Montaner J
[Ad] Endereço:From the Neurovascular Research Laboratory, Vall d'Hebron Institut de Recerca (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Spain (A.B., A.P., D.G., T.G.-B., J.M.); Stroke Unit, Hospital Universitari Germans Trias i Pujol, Barcelona, Spain (E.L.-C., M.H.-P., M.M., A
[Ti] Título:Blood Biomarkers for the Early Diagnosis of Stroke: The Stroke-Chip Study.
[So] Source:Stroke;48(9):2419-2425, 2017 Sep.
[Is] ISSN:1524-4628
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Stroke diagnosis could be challenging in the acute phase. We aimed to develop a blood-based diagnostic tool to differentiate between real strokes and stroke mimics and between ischemic and hemorrhagic strokes in the hyperacute phase. METHODS: The Stroke-Chip was a prospective, observational, multicenter study, conducted at 6 Stroke Centers in Catalonia. Consecutive patients with suspected stroke were enrolled within the first 6 hours after symptom onset, and blood samples were drawn immediately after admission. A 21-biomarker panel selected among previous results and from the literature was measured by immunoassays. Outcomes were differentiation between real strokes and stroke mimics and between ischemic and hemorrhagic strokes. Predictive models were developed by combining biomarkers and clinical variables in logistic regression models. Accuracy was evaluated with receiver operating characteristic curves. RESULTS: From August 2012 to December 2013, 1308 patients were included (71.9% ischemic, 14.8% stroke mimics, and 13.3% hemorrhagic). For stroke versus stroke mimics comparison, no biomarker resulted included in the logistic regression model, but it was only integrated by clinical variables, with a predictive accuracy of 80.8%. For ischemic versus hemorrhagic strokes comparison, NT-proBNP (N-Terminal Pro-B-Type Natriuretic Peptide) >4.9 (odds ratio, 2.40; 95% confidence interval, 1.55-3.71; <0.0001) and endostatin >4.7 (odds ratio, 2.02; 95% confidence interval, 1.19-3.45; =0.010), together with age, sex, blood pressure, stroke severity, atrial fibrillation, and hypertension, were included in the model. Predictive accuracy was 80.6%. CONCLUSIONS: The studied biomarkers were not sufficient for an accurate differential diagnosis of stroke in the hyperacute setting. Additional discovery of new biomarkers and improvement on laboratory techniques seem necessary for achieving a molecular diagnosis of stroke.
[Mh] Termos MeSH primário: Isquemia Encefálica/sangue
Hemorragia Cerebral/sangue
Acidente Vascular Cerebral/sangue
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Amina Oxidase (contendo Cobre)/sangue
Apolipoproteína C-III/sangue
Biomarcadores/sangue
Isquemia Encefálica/diagnóstico
Estudos de Casos e Controles
Caspase 3/sangue
Moléculas de Adesão Celular/sangue
Hemorragia Cerebral/diagnóstico
Quimiocina CXCL1/sangue
Endostatinas/sangue
Proteína Ligante Fas/sangue
Feminino
Produtos de Degradação da Fibrina e do Fibrinogênio/metabolismo
Fibronectinas/sangue
Proteínas de Choque Térmico HSC70/sangue
Seres Humanos
Proteína 3 de Ligação a Fator de Crescimento Semelhante à Insulina/sangue
Subunidade gama Comum de Receptores de Interleucina/sangue
Interleucina-17/sangue
Interleucina-6/sangue
Modelos Logísticos
Masculino
Metaloproteinase 9 da Matriz/sangue
Meia-Idade
Peptídeo Natriurético Encefálico/sangue
Fator de Crescimento Neural/sangue
Moléculas de Adesão de Célula Nervosa/sangue
Razão de Chances
Fragmentos de Peptídeos/sangue
Fosfopiruvato Hidratase/sangue
Estudos Prospectivos
Curva ROC
Receptores Tipo I de Fatores de Necrose Tumoral/sangue
Subunidade beta da Proteína Ligante de Cálcio S100/sangue
Acidente Vascular Cerebral/diagnóstico
Fator de von Willebrand/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Apolipoprotein C-III); 0 (Biomarkers); 0 (Cell Adhesion Molecules); 0 (Chemokine CXCL1); 0 (Endostatins); 0 (FASLG protein, human); 0 (Fas Ligand Protein); 0 (Fibrin Fibrinogen Degradation Products); 0 (Fibronectins); 0 (HSC70 Heat-Shock Proteins); 0 (HSPA8 protein, human); 0 (IGFBP3 protein, human); 0 (IL17A protein, human); 0 (IL2RG protein, human); 0 (IL6 protein, human); 0 (Insulin-Like Growth Factor Binding Protein 3); 0 (Interleukin Receptor Common gamma Subunit); 0 (Interleukin-17); 0 (Interleukin-6); 0 (NGF protein, human); 0 (Neural Cell Adhesion Molecules); 0 (Peptide Fragments); 0 (Receptors, Tumor Necrosis Factor, Type I); 0 (S100 Calcium Binding Protein beta Subunit); 0 (S100B protein, human); 0 (fibrin fragment D); 0 (pro-brain natriuretic peptide (1-76)); 0 (von Willebrand Factor); 114471-18-0 (Natriuretic Peptide, Brain); 9061-61-4 (Nerve Growth Factor); EC 1.4.3.21 (AOC3 protein, human); EC 1.4.3.21 (Amine Oxidase (Copper-Containing)); EC 3.4.22.- (CASP3 protein, human); EC 3.4.22.- (Caspase 3); EC 3.4.24.35 (MMP9 protein, human); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 4.2.1.11 (Phosphopyruvate Hydratase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1161/STROKEAHA.117.017076


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[PMID]:28598289
[Au] Autor:Lee CT; Zhou Y; Roy-Choudhury K; Siamakpour-Reihani S; Young K; Hoang P; Kirkpatrick JP; Chi JA; Dewhirst MW; Horton JK
[Ad] Endereço:Department of a Radiation Oncology, Duke University Medical Center, Durham, North Carolina.
[Ti] Título:Subtype-Specific Radiation Response and Therapeutic Effect of FAS Death Receptor Modulation in Human Breast Cancer.
[So] Source:Radiat Res;188(2):169-180, 2017 Aug.
[Is] ISSN:1938-5404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Breast cancer is the most common malignancy diagnosed among women and represents a heterogeneous group of subtypes. Radiation therapy is a critical component of treatment for breast cancer patients. However, little is known about radiation response among these intrinsic subtypes. In previous studies, we identified a significant induction of FAS after irradiation in biologically favorable breast cancer patients and breast cancer cell lines. Here, we expanded our study and investigated radiation response in a mouse model of breast cancer. MCF7 (luminal), HCC1954 (HER2 ) or SUM159 (basal) cells were implanted orthotopically into the dorsal mammary fat pad of nude mice. These mice were then treated with different doses of radiation to assess tumor growth control. We further investigated the therapeutic effect of FAS modulation by silencing FAS in radiation-responsive tumors and injecting FAS agonist antibody into radiation-resistant tumors. Exposure to radiation inhibited MCF7, and to a lesser extent HCC1954 tumor growth in a dose-dependent manner. In contrast, SUM159 tumors were resistant to radiation. The estimated TCD values were 19.3 Gy for MCF7 and 44.9 Gy for SUM159. Radiation induced FAS expression in MCF7 tumors, but not SUM159 tumors. We found that silencing of FAS did not negatively impact radiation response in MCF7 tumors, possibly due to compensation by other apoptotic pathways. On the other hand, FAS activating antibody in combination with radiation treatment delayed SUM159 and HCC1954 tumor growth. However, it did not reach statistical significance compared to radiation treatment alone. Our results suggest that there is intrinsic variation in radiation response among breast cancer subtypes. FAS activation concurrent with radiation slows tumor growth in the radiation-resistant subtypes, but the effect was not significant. Alternative subtype-specific modulators of radiation response are under investigation.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Neoplasias da Mama/radioterapia
Receptor fas/metabolismo
[Mh] Termos MeSH secundário: Animais
Neoplasias da Mama/patologia
Linhagem Celular Tumoral
Transformação Celular Neoplásica
Proteína Ligante Fas/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica/efeitos da radiação
Inativação Gênica
Seres Humanos
Camundongos
Tolerância a Radiação
Resultado do Tratamento
Receptor fas/deficiência
Receptor fas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fas Ligand Protein); 0 (fas Receptor)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM; S
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE
[do] DOI:10.1667/RR14664.1


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[PMID]:28579554
[Au] Autor:Nabhani S; Schipp C; Miskin H; Levin C; Postovsky S; Dujovny T; Koren A; Harlev D; Bis AM; Auer F; Keller B; Warnatz K; Gombert M; Ginzel S; Borkhardt A; Stepensky P; Fischer U
[Ad] Endereço:Department of Pediatric Oncology, Hematology and Clinical Immunology, University Children's Hospital, Medical Faculty, Heinrich-Heine-University Düsseldorf, Germany.
[Ti] Título:STAT3 gain-of-function mutations associated with autoimmune lymphoproliferative syndrome like disease deregulate lymphocyte apoptosis and can be targeted by BH3 mimetic compounds.
[So] Source:Clin Immunol;181:32-42, 2017 Aug.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Autoimmune lymphoproliferative syndrome (ALPS) is typically caused by mutations in genes of the extrinsic FAS mediated apoptotic pathway, but for about 30% of ALPS-like patients the genetic diagnosis is lacking. We analyzed 30 children with ALPS-like disease of unknown cause and identified two dominant gain-of-function mutations of the Signal Transducer And Activator Of Transcription 3 (STAT3, p.R278H, p.M394T) leading to increased transcriptional activity. Hyperactivity of STAT3, a known repressor of FAS, was associated with decreased FAS-mediated apoptosis, mimicking ALPS caused by FAS mutations. Expression of BCL2 family proteins, further targets of STAT3 and regulators of the intrinsic apoptotic pathway, was disturbed. Cells with hyperactive STAT3 were consequently more resistant to intrinsic apoptotic stimuli and STAT3 inhibition alleviated this effect. Importantly, STAT3-mutant cells were more sensitive to death induced by the BCL2-inhibitor ABT-737 indicating a dependence on anti-apoptotic BCL2 proteins and potential novel therapeutic options.
[Mh] Termos MeSH primário: Apoptose/genética
Síndrome Linfoproliferativa Autoimune/genética
Fator de Transcrição STAT3/genética
[Mh] Termos MeSH secundário: Compostos de Bifenilo
Hidroxitolueno Butilado/análogos & derivados
Estudos de Casos e Controles
Pré-Escolar
Ensaio de Imunoadsorção Enzimática
Família
Proteína Ligante Fas/metabolismo
Feminino
Perfilação da Expressão Gênica
Mutação em Linhagem Germinativa
Seres Humanos
Immunoblotting
Imunofenotipagem
Leucócitos Mononucleares
Linfócitos
Nitrofenóis
Piperazinas
Proteínas Proto-Oncogênicas c-bcl-2/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Análise de Sequência de DNA
Sulfonamidas
Linfócitos T/efeitos dos fármacos
Linfócitos T/metabolismo
Receptor fas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ABT-737); 0 (Biphenyl Compounds); 0 (FAS protein, human); 0 (FASLG protein, human); 0 (Fas Ligand Protein); 0 (Nitrophenols); 0 (Piperazines); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (Sulfonamides); 0 (fas Receptor); 1P9D0Z171K (Butylated Hydroxytoluene); 728-39-2 (BH 3)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE



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