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[PMID]:28608562
[Au] Autor:Chaudhuri S; Singh MK; Bhattacharya D; Datta A; Hazra I; Mondal S; Faruk Sk Md O; Ronsard L; Ghosh TK; Chaudhuri S
[Ad] Endereço:Department of Laboratory Medicine, Cellular and Molecular Immunology Lab, School of Tropical Medicine, Kolkata, West Bengal 700073, India.
[Ti] Título:T11TS immunotherapy repairs PI3K-AKT signaling in T-cells: Clues toward enhanced T-cell survival in rat glioma model.
[So] Source:J Cell Physiol;233(2):759-770, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Malignant glioma is the most fatal of astrocytic lineage tumors despite therapeutic advances. Onset and progression of gliomas is accompanied by severe debilitation of T-cell defense and T-cell survival. One of the chief contributors to T-cell survival downstream of activation is the PI3K-AKT pathway. Our prior studies showed that the novel immunotherapeutic molecule T11-target structure (T11TS) blocks T-cell apoptosis in glioma. We also showed activation of immunological synapse components and calcineurin-NFAT pathway following T11TS immunotherapy of glioma-bearing rats. This lead to investigations whether such T-cell activation upon T11TS therapy translates into activation of downstream PI3K/AKT signals which may be related to observed blockade of T-cell apoptosis. For the purpose, we assessed by flowcytometry and immunoblotting, expressions of PI3K, PDK1, AKT, p-AKT, and PTEN in splenic T-cells of normal, experimentally-induced glioma-bearing rats and glioma-bearing rats receiving first, second and third doses of T11TS. We also determined comparative nuclear translocation of NF-κB across groups. We found significant increases in T-cell expressions of PDK1, PI3K, and p-AKT in T11TS-treated animal groups compared to sharp downregulations in glioma. AKT levels remained unchanged across groups. PTEN levels declined sharply after T11TS immunotherapy. T11TS also caused enhanced NF-κB translocation to the T-cell nucleus compared to glioma group. Results showed heightened activation of the PI3K-AKT pathway in glioma-bearing rats following T11TS immunotherapy. These results illustrate the novel role of T11TS immunotherapy in ameliorating the PI3K pathway in T-cells in glioma-bearing animals to enhance T-cell survival, according greater defense against glioma. The study thus has far-reaching clinical outcomes.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Neoplasias Encefálicas/tratamento farmacológico
Antígenos CD58/farmacologia
Glioma/tratamento farmacológico
Imunoterapia/métodos
Fosfatidilinositol 3-Quinase/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Linfócitos T/efeitos dos fármacos
Evasão Tumoral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Proteínas Quinases Dependentes de 3-Fosfoinositídeo/metabolismo
Transporte Ativo do Núcleo Celular
Animais
Neoplasias Encefálicas/enzimologia
Neoplasias Encefálicas/imunologia
Neoplasias Encefálicas/patologia
Antígenos CD28/imunologia
Antígenos CD28/metabolismo
Sobrevivência Celular
Etilnitrosoureia
Feminino
Glioma/enzimologia
Glioma/imunologia
Glioma/patologia
Masculino
NF-kappa B/metabolismo
PTEN Fosfo-Hidrolase/metabolismo
Fosforilação
Ratos
Transdução de Sinais/efeitos dos fármacos
Linfócitos T/enzimologia
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (CD28 Antigens); 0 (CD58 Antigens); 0 (NF-kappa B); 0 (T11TS protein, sheep); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (3-Phosphoinositide-Dependent Protein Kinases); EC 2.7.11.1 (Pdpk1 protein, rat); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (Pten protein, rat); P8M1T4190R (Ethylnitrosourea)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.26047


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[PMID]:28601281
[Au] Autor:Liu J; Shi Z; Lian Z; Chen H; Zhang Q; Feng H; Miao X; Du Q; Zhou H
[Ad] Endereço:Department of Neurology, West China Hospital, Sichuan University, Guo Xuexiang #37, Chengdu 610041, China.
[Ti] Título:Association of CD58 gene polymorphisms with NMO spectrum disorders in a Han Chinese population.
[So] Source:J Neuroimmunol;309:23-30, 2017 Aug 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:This study aimed to perform a comprehensive assessment of the association between CD58 polymorphisms and the risk of neuromyelitis optica spectrum disorders (NMOSD) in a Han Chinese population. Nine single-nucleotide polymorphisms (SNPs) were genotyped in 230 NMOSD patients and 487 healthy controls. Five SNPs were significantly associated with an increased risk of NMOSD (rs2300747, rs1335532, rs56302466, rs1016140, and rs12044852). The haplotype TAGCCCAA significantly increased the risk of NMOSD, while TATTACGG reduced the risk. In conclusion, this study identified a new NMOSD susceptibility variant, rs56302466, and suggested that CD58 polymorphisms are associated with the risk of NMOSD in Han Chinese.
[Mh] Termos MeSH primário: Grupo com Ancestrais do Continente Asiático/genética
Antígenos CD58/genética
Estudos de Associação Genética/métodos
Neuromielite Óptica/epidemiologia
Neuromielite Óptica/genética
Polimorfismo de Nucleotídeo Único/genética
[Mh] Termos MeSH secundário: Adulto
Feminino
Variação Genética/genética
Seres Humanos
Masculino
Meia-Idade
Neuromielite Óptica/diagnóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD58 Antigens)
[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:170612
[St] Status:MEDLINE


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[PMID]:27581603
[Au] Autor:Duggan MC; Jochems C; Donahue RN; Richards J; Karpa V; Foust E; Paul B; Brooks T; Tridandapani S; Olencki T; Pan X; Lesinski GB; Schlom J; Carson Iii WE
[Ad] Endereço:Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
[Ti] Título:A phase I study of recombinant (r) vaccinia-CEA(6D)-TRICOM and rFowlpox-CEA(6D)-TRICOM vaccines with GM-CSF and IFN-α-2b in patients with CEA-expressing carcinomas.
[So] Source:Cancer Immunol Immunother;65(11):1353-1364, 2016 Nov.
[Is] ISSN:1432-0851
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Prime-boost vaccination with recombinant (r) vaccinia(V)-CEA(6D)-TRICOM (triad of co-stimulatory molecules B7.1, ICAM-1 and LFA-3) and rFowlpox(F)-CEA(6D)-TRICOM infect antigen-presenting cells and direct expression of co-stimulatory molecules. We hypothesized that co-administration of vaccine with GM-CSF and interferon alpha (IFN-α) would have efficacy in CEA-expressing cancers. Patients with CEA-expressing cancers received the rV-CEA(6D)-TRICOM vaccine subcutaneously (s.c.) on day 1 followed by GM-CSF s.c. to the injection site on days 1-4. In Cycle 1, patients received thrice weekly s.c. injections of IFN-α-2b the week after rV-CEA(6D)-TRICOM. In Cycles 2-4, patients received thrice weekly s.c. injections of IFN-α-2b the same week that rF-CEA(6D)-TRICOM was given. The first cohort received no IFN followed by dose escalation of IFN-α in subsequent cohorts. Thirty-three patients were accrued (mean 59.8 years). Grade 3 toxicities included fatigue and hyperglycemia. Grade 4-5 adverse events (unrelated to treatment) were confusion (1), elevated aspartate transaminase (AST)/alanine transaminase (ALT) (1), and sudden death (1). No patients had a partial response, and eight patients exhibited stable disease of ≥3 months. Median progression-free survival and overall survival (OS) were 1.8 and 6.3 months, respectively. Significantly higher serum CD27 levels were observed after vaccine therapy (p = 0.006 post 1-2 cycles, p = 0.003 post 3 cycles, p = 0.03 post 4-7 cycles) and 42 % of patients assayed developed CEA-specific T cell responses. Pre-treatment levels of myeloid-derived suppressor cells correlated with overall survival (p = 0.04). Administration of IFN-α led to significantly increased OS (p = 0.02) compared to vaccine alone. While the vaccine regimen produced no clinical responses, IFN-α administration was associated with improved survival.
[Mh] Termos MeSH primário: Vacinas Anticâncer/imunologia
Antígeno Carcinoembrionário/imunologia
Neoplasias Colorretais/terapia
Fator Estimulador de Colônias de Granulócitos e Macrófagos/administração & dosagem
Interferon-alfa/administração & dosagem
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Antígeno B7-H1/genética
Antígenos CD58/genética
Antígeno Carcinoembrionário/genética
Neoplasias Colorretais/imunologia
Neoplasias Colorretais/mortalidade
Feminino
Seres Humanos
Hiperglicemia/etiologia
Molécula 1 de Adesão Intercelular/genética
Masculino
Meia-Idade
Análise de Sobrevida
Resultado do Tratamento
Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/metabolismo
Vacinação
Vacinas Sintéticas
Vírus Vaccinia/genética
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (B7-H1 Antigen); 0 (CD274 protein, human); 0 (CD58 Antigens); 0 (Cancer Vaccines); 0 (Carcinoembryonic Antigen); 0 (Interferon-alpha); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 7); 0 (Vaccines, Synthetic); 126547-89-5 (Intercellular Adhesion Molecule-1); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
[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:160902
[St] Status:MEDLINE


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[PMID]:27469079
[Au] Autor:Rölle A; Halenius A; Ewen EM; Cerwenka A; Hengel H; Momburg F
[Ad] Endereço:Clinical Cooperation Unit Applied Tumor Immunity, Antigen Presentation & T/NK Cell Activation Group, German Cancer Research Center (DKFZ/D121), Heidelberg, Germany. a.roelle@dkfz.de.
[Ti] Título:CD2-CD58 interactions are pivotal for the activation and function of adaptive natural killer cells in human cytomegalovirus infection.
[So] Source:Eur J Immunol;46(10):2420-2425, 2016 Oct.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The existence and expansion of adaptive NK-cell subsets have been linked to HCMV infection. Phenotypically, a majority of adaptive NK cells expresses the activating receptor NKG2C and CD57. Some of the molecular factors driving the expansion of NKG2C CD57 NK cells in HCMV infection have been identified. The direct interaction of adaptive NK cells with HCMV-infected cells, preceding the expansion, however, remains less studied. Recently, adaptive NK cells were reported to express higher levels of the co-activating receptor CD2. We explored whether CD2 was directly involved in the response of adaptive NK cells to HCMV. In a co-culture system of human PBMCs and productively infected fibroblasts, we observed an upregulation of CD69, CD25, and HLA-DR on all NK cells. However, only in adaptive NK cells was this increase largely blocked by antibodies against CD2 and CD58. Functionally, this blockade also resulted in diminished production of IFN-γ and TNF-α by adaptive human NK cells in response to HCMV-infected cells. Our results demonstrate that binding of CD2 to upregulated CD58 on infected cells is a critical event for antibody-mediated activation and subsequent effector functions of adaptive NKG2C CD57 NK cells during the antiviral response.
[Mh] Termos MeSH primário: Antígenos CD2/metabolismo
Antígenos CD58/metabolismo
Infecções por Citomegalovirus/imunologia
Citomegalovirus/imunologia
Fibroblastos/imunologia
Células Matadoras Naturais/imunologia
[Mh] Termos MeSH secundário: Imunidade Adaptativa
Anticorpos/metabolismo
Proliferação Celular
Células Cultivadas
Fibroblastos/virologia
Seres Humanos
Interferon gama/metabolismo
Ativação Linfocitária
Ligação Proteica
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (CD2 Antigens); 0 (CD58 Antigens); 0 (Tumor Necrosis Factor-alpha); 82115-62-6 (Interferon-gamma)
[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:160730
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201646492


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[PMID]:27467287
[Au] Autor:Abdul Razak FR; Diepstra A; Visser L; van den Berg A
[Ad] Endereço:Department of Pathology and Medical Biology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
[Ti] Título:CD58 mutations are common in Hodgkin lymphoma cell lines and loss of CD58 expression in tumor cells occurs in Hodgkin lymphoma patients who relapse.
[So] Source:Genes Immun;17(6):363-6, 2016 Sep.
[Is] ISSN:1476-5470
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:CD58 is involved in immune recognition of tumor cells via binding of the CD2 receptor expressed on cytotoxic T cells. In diffuse large B-cell lymphoma, mutations of the CD58 gene are reported to contribute to immune evasion of the tumor cells. We previously showed CD58 mutations in three Hodgkin lymphoma (HL) cell lines by whole-exome sequencing. In this study, we confirmed the mutations by Sanger sequencing at the DNA and RNA level and showed low levels or total loss of CD58 mRNA expression in two of the three cell lines. CD58 protein expression as determined by flow cytometry, western blotting and immunohistochemistry was absent in all three mutated HL cell lines. In primary tissue samples, loss of CD58 expression was observed in 11% of the patients who relapse. These data suggest that loss of CD58 is a potential immune escape mechanism of HL tumor cells, especially in clinically aggressive disease.
[Mh] Termos MeSH primário: Antígenos CD58/genética
Doença de Hodgkin/genética
Mutação
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Doença de Hodgkin/imunologia
Seres Humanos
Recidiva
Evasão Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD58 Antigens)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160729
[St] Status:MEDLINE
[do] DOI:10.1038/gene.2016.30


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[PMID]:27383875
[Au] Autor:Burnusuzov HA; Spasova MI; Murdjeva MA; Stoyanova AA; Mumdziev IN; Kaleva VI; Belcheva MI; Bosheva MN
[Ad] Endereço:Department of Pediatrics and Medical Genetics, Medical University of Plovdiv, Plovdiv, Bulgaria
[Ti] Título:Immunophenotypic Modulation of the Blast Cells in Childhood Acute Lymphoblastic Leukemia Minimal Residual Disease Detection.
[So] Source:Folia Med (Plovdiv);58(1):28-35, 2016 03 01.
[Is] ISSN:0204-8043
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Early clearance of leukemic cells during induction therapy of childhood acute lymphoblastic leukemia (ALL) is a basis for treatment optimization. Currently, the most widely used methods for the detection of minute residual malignant cells in the bone marrow and/or peripheral blood, minimal residual disease (MRD), are PCR and flow cytometry (FCM). Immunophenotypic modulation (IM) is a well known factor that can hamper the accurate FCM analysis. AIM: To report the IM detected by 8-color FCM during the BFM-type remission induction in 24 consecutive MRD-positive samples of children with B-cell precursor ALL and the possible implications for MRD detection. PATIENTS AND METHODS: Between 2010 and 2012 we prospectively followed up the MRD on days 15 and 33 of induction treatment in bone marrow (BM) samples and on day 8 in peripheral blood (PB). The IM was assessed by comparative analyses of the changes in the mean fluorescence intensity of 7 highly relevant antigens expressed by the leukemic cells and normal B-lymphocytes. RESULTS: IM occurred, to different extents, in all analyzed day 15 BM and in most day 33 BM samples. Statistically significant changes in the MFI-levels of four CDs expressed by the leukemic blasts were observed: downmodulation of CD10, CD19 and CD34 and upmodulation of CD20. No changes in the expression of CD38, CD58 and CD45 were noticed. CONCLUSIONS: Measuring the MRD by standardized 8-color flow cytometry helps improve the monitoring of the disease, leading to better therapeutic results. However, the IM of the different antigens expressed by the leukemic blasts should be taken into consideration and cautiously analyzed.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Células da Medula Óssea/imunologia
Leucemia-Linfoma Linfoblástico de Células Precursoras B/diagnóstico
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase 1/imunologia
Adolescente
Antígenos CD19/imunologia
Antígenos CD20/imunologia
Antígenos CD34/imunologia
Medula Óssea
Antígenos CD58/imunologia
Criança
Pré-Escolar
Feminino
Citometria de Fluxo
Seres Humanos
Imunofenotipagem
Quimioterapia de Indução
Lactente
Antígenos Comuns de Leucócito/imunologia
Masculino
Glicoproteínas de Membrana/imunologia
Neoplasia Residual/diagnóstico
Neoplasia Residual/tratamento farmacológico
Neoplasia Residual/imunologia
Neprilisina/imunologia
Leucemia-Linfoma Linfoblástico de Células Precursoras B/tratamento farmacológico
Leucemia-Linfoma Linfoblástico de Células Precursoras B/imunologia
Leucemia-Linfoma Linfoblástico de Células Precursoras/diagnóstico
Leucemia-Linfoma Linfoblástico de Células Precursoras/tratamento farmacológico
Leucemia-Linfoma Linfoblástico de Células Precursoras/imunologia
Estudos Prospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD19); 0 (Antigens, CD20); 0 (Antigens, CD34); 0 (CD19 molecule, human); 0 (CD58 Antigens); 0 (Membrane Glycoproteins); EC 3.1.3.48 (Leukocyte Common Antigens); EC 3.1.3.48 (PTPRC protein, human); EC 3.2.2.5 (CD38 protein, human); EC 3.2.2.6 (ADP-ribosyl Cyclase 1); EC 3.4.24.11 (Neprilysin)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171127
[Lr] Data última revisão:
171127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160708
[St] Status:MEDLINE


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[PMID]:27337048
[Au] Autor:Sable R; Durek T; Taneja V; Craik DJ; Pallerla S; Gauthier T; Jois S
[Ad] Endereço:Basic Pharmaceutical Sciences, School of Pharmacy, University of Louisiana at Monroe , Monroe, Louisiana 71201, United States.
[Ti] Título:Constrained Cyclic Peptides as Immunomodulatory Inhibitors of the CD2:CD58 Protein-Protein Interaction.
[So] Source:ACS Chem Biol;11(8):2366-74, 2016 Aug 19.
[Is] ISSN:1554-8937
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The interaction between the cell-cell adhesion proteins CD2 and CD58 plays a crucial role in lymphocyte recruitment to inflammatory sites, and inhibitors of this interaction have potential as immunomodulatory drugs in autoimmune diseases. Peptides from the CD2 adhesion domain were designed to inhibit CD2:CD58 interactions. To improve the stability of the peptides, ß-sheet epitopes from the CD2 region implicated in CD58 recognition were grafted into the cyclic peptide frameworks of sunflower trypsin inhibitor and rhesus theta defensin. The designed multicyclic peptides were evaluated for their ability to modulate cell-cell interactions in three different cell adhesion assays, with one candidate, SFTI-a, showing potent activity in the nanomolar range (IC50: 51 nM). This peptide also suppresses the immune responses in T cells obtained from mice that exhibit the autoimmune disease rheumatoid arthritis. SFTI-a was resistant to thermal denaturation, as judged by circular dichroism spectroscopy and mass spectrometry, and had a half-life of ∼24 h in human serum. Binding of this peptide to CD58 was predicted by molecular docking studies and experimentally confirmed by surface plasmon resonance experiments. Our results suggest that cyclic peptides from natural sources are promising scaffolds for modulating protein-protein interactions that are typically difficult to target with small-molecule compounds.
[Mh] Termos MeSH primário: Adjuvantes Imunológicos/farmacologia
Antígenos CD2/metabolismo
Antígenos CD58/metabolismo
Peptídeos Cíclicos/farmacologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Adesão Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Dicroísmo Circular
Seres Humanos
Espectrometria de Massas
Camundongos
Modelos Moleculares
Ressonância Magnética Nuclear Biomolecular
Peptídeos Cíclicos/química
Ligação Proteica
Ressonância de Plasmônio de Superfície
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (CD2 Antigens); 0 (CD58 Antigens); 0 (Peptides, Cyclic)
[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:160624
[St] Status:MEDLINE
[do] DOI:10.1021/acschembio.6b00486


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[PMID]:26930456
[Au] Autor:Li XM; Zhang LP; Wang YZ; Lu AD; Chang Y; Zhu HH; Qin YZ; Lai YY; Kong Y; Huang XJ; Liu YR
[Ad] Endereço:Peking University People's Hospital, Peking University Institute of Hematology, Beijing, China.
[Ti] Título:CD38+ CD58- is an independent adverse prognostic factor in paediatric Philadelphia chromosome negative B cell acute lymphoblastic leukaemia patients.
[So] Source:Leuk Res;43:33-8, 2016 Apr.
[Is] ISSN:1873-5835
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:To explore new risk predictors for a high risk of relapse in Philadelphia chromosome negative (Ph-) B cell acute lymphoblastic leukaemia (B-ALL) patients, 196 paediatric Ph- B-ALL patients (≤ 18 years) were retrospectively analysed. We mainly focus on investigating the prognostic value of CD38 and CD58 expression in leukemic blasts in these patients by four colour flow cytometry. The CD38+ CD58- group (n=16) had a higher relapse rate, a shorter 3-year event-free survival (EFS) and overall survival (OS) than the CD38+ CD58+ group (n=157; 31.3% vs 10.2%, P=0.04; 52.4% vs 92.3%, P<0.01; 32.5% vs 91.0%, P=0.01); CD38+ CD58- was an independent adverse prognostic predictor for relapse (hazard ratio [HR], 0.203; 95%CI, 0.063-0.656; P=0.01), 3-year EFS (HR, 0.091; 95%CI, 0.023-0.355; P<0.01) and OS (HR, 0.102; 95%CI, 0.026-0.3971; P<0.01) in this cohort, as determined by Cox multivariate analysis. We identified, for the first time, a higher risk population of paediatric Ph- B-ALL patients with CD38+ CD58- who had a higher relapse risk and a shorter survival. Our results may allow better risk stratification and individualized treatment.
[Mh] Termos MeSH primário: ADP-Ribosil Ciclase 1/sangue
Antígenos CD58
Proteínas de Neoplasias/sangue
Cromossomo Filadélfia
Leucemia-Linfoma Linfoblástico de Células Precursoras B/sangue
Leucemia-Linfoma Linfoblástico de Células Precursoras B/mortalidade
[Mh] Termos MeSH secundário: Adolescente
Criança
Pré-Escolar
Intervalo Livre de Doença
Feminino
Seres Humanos
Lactente
Recém-Nascido
Masculino
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD58 Antigens); 0 (Neoplasm Proteins); EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160302
[St] Status:MEDLINE


  9 / 629 MEDLINE  
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[PMID]:26794910
[Au] Autor:McArdel SL; Terhorst C; Sharpe AH
[Ad] Endereço:Department of Microbiology and Immunobiology, Evergrande Center for Immunologic Diseases, Harvard Medical School, Boston, MA, USA.
[Ti] Título:Roles of CD48 in regulating immunity and tolerance.
[So] Source:Clin Immunol;164:10-20, 2016 Mar.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD48, a member of the signaling lymphocyte activation molecule family, participates in adhesion and activation of immune cells. Although constitutively expressed on most hematopoietic cells, CD48 is upregulated on subsets of activated cells. CD48 can have activating roles on T cells, antigen presenting cells and granulocytes, by binding to CD2 or bacterial FimH, and through cell intrinsic effects. Interactions between CD48 and its high affinity ligand CD244 are more complex, with both stimulatory and inhibitory outcomes. CD244:CD48 interactions regulate target cell lysis by NK cells and CTLs, which are important for viral clearance and regulation of effector/memory T cell generation and survival. Here we review roles of CD48 in infection, tolerance, autoimmunity, and allergy, as well as the tools used to investigate this receptor. We discuss stimulatory and regulatory roles for CD48, its potential as a therapeutic target in human disease, and current challenges to investigation of this immunoregulatory receptor.
[Mh] Termos MeSH primário: Antígenos CD/imunologia
[Mh] Termos MeSH secundário: Animais
Autoimunidade
Antígeno CD48
Antígenos CD58/imunologia
Seres Humanos
Tolerância Imunológica
Ligantes
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Nm] Nome de substância:
0 (Antigens, CD); 0 (CD48 Antigen); 0 (CD48 protein, human); 0 (CD58 Antigens); 0 (Ligands)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160123
[St] Status:MEDLINE


  10 / 629 MEDLINE  
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[PMID]:26600503
[Au] Autor:Niu JX; Guo HP; Gan HM; Bao LD; Ren JJ
[Ad] Endereço:Department of General Surgery, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
[Ti] Título:Effect of luteolin on gene expression in mouse H22 hepatoma cells.
[So] Source:Genet Mol Res;14(4):14448-56, 2015 Nov 19.
[Is] ISSN:1676-5680
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:The purpose of our study was to observe the effects of luteolin on the expression of the genes ICAM-1, LFA-3, and PCNA in H22 hepatoma tissue. Sixty ICR (Institute of Cancer Research) mice with H22 hepatoma were randomly divided into five groups: a normal saline control group, low-, medium-, and high-dose luteolin groups, and a cyclophosphamide group. The mice were euthanized the day after administration withdrawal and subcutaneous tumor tissue was extracted. Quantitative fluorescence RT-PCR was used to detect the expression of ICAM-1, LFA-3, and PCNA in H22 hepatoma tissue in the mice. Luteolin was found to up-regulate the expression of ICAM-1 in H22 hepatoma tissue, of which the middle-dose group had the most obvious effect, showing a significant difference (P < 0.01) as compared to the normal saline group. Each dose group of luteolin significantly down-regulated the expression of LFA-3 in H22 hepatoma tissue, showing significant differences as compared to the saline control group (P < 0.01). The medium- and high-dose luteolin groups significantly reduced the expression of PCNA in H22 hepatoma tissue of ICR mice, where the effect of the high-dose group was the most obvious, and the difference between the two luteolin groups and the normal saline group was statistically significant (P < 0.01). Luteolin may inhibit tumor angiogenesis and tumor cell proliferation by down-regulation of LFA- 3 and PCNA and up-regulation of ICAM-1 in tumor tissue of tumor-bearing mice, thereby achieving its anti-tumor effect.
[Mh] Termos MeSH primário: Antígenos CD58/biossíntese
Carcinoma Hepatocelular/genética
Molécula 1 de Adesão Intercelular/biossíntese
Neoplasias Hepáticas/genética
Neovascularização Patológica/genética
Antígeno Nuclear de Célula em Proliferação/biossíntese
[Mh] Termos MeSH secundário: Animais
Antígenos CD58/genética
Carcinoma Hepatocelular/tratamento farmacológico
Carcinoma Hepatocelular/patologia
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Fluoruracila/administração & dosagem
Regulação Neoplásica da Expressão Gênica
Molécula 1 de Adesão Intercelular/genética
Neoplasias Hepáticas/tratamento farmacológico
Neoplasias Hepáticas/patologia
Luteolina/administração & dosagem
Camundongos
Neovascularização Patológica/tratamento farmacológico
Neovascularização Patológica/patologia
Antígeno Nuclear de Célula em Proliferação/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD58 Antigens); 0 (Proliferating Cell Nuclear Antigen); 126547-89-5 (Intercellular Adhesion Molecule-1); KUX1ZNC9J2 (Luteolin); U3P01618RT (Fluorouracil)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151125
[St] Status:MEDLINE
[do] DOI:10.4238/2015.November.18.7



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