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Pesquisa : A11.118.637.555.283.500 [Categoria DeCS]
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  1 / 2913 MEDLINE  
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[PMID]:28214839
[Au] Autor:Ma W; Wu L; Zhou F; Hong Z; Yuan Y; Liu Z
[Ti] Título:T Cell-Associated Immunotherapy for Hepatocellular Carcinoma.
[So] Source:Cell Physiol Biochem;41(2):609-622, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Hepatocellular carcinoma (HCC) is one of the most common malignant diseases worldwide with limited therapeutic options. Accumulating evidences suggest that immunotherapy could be a promising option for treating HCC. T cell-associated immunotherapy lights up the hope for the improvement of complementary approach to conventional HCC treatments, which needs further research to consummate the clinical consequences. The present work reviewed several T cells associated cellular immunotherapies for HCC, including immune checkpoint blockade, gene-engineered T cells, bispecific T cell engagers, and so on. We also analyzed how these immunotherapies can mediate tumor cell eradication and evaluated their superiority or insufficiency.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/terapia
Imunoterapia
Neoplasias Hepáticas/terapia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Carcinoma Hepatocelular/patologia
Seres Humanos
Células Matadoras Ativadas por Linfocina/citologia
Células Matadoras Ativadas por Linfocina/imunologia
Células Matadoras Ativadas por Linfocina/metabolismo
Neoplasias Hepáticas/patologia
Receptores de Antígenos/genética
Receptores de Antígenos/metabolismo
Receptores de Antígenos de Linfócitos T/genética
Receptores de Antígenos de Linfócitos T/metabolismo
Anticorpos de Cadeia Única/genética
Anticorpos de Cadeia Única/metabolismo
Linfócitos T/citologia
Linfócitos T/metabolismo
Linfócitos T Citotóxicos/citologia
Linfócitos T Citotóxicos/imunologia
Linfócitos T Citotóxicos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Antigen); 0 (Receptors, Antigen, T-Cell); 0 (Single-Chain Antibodies)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170220
[St] Status:MEDLINE
[do] DOI:10.1159/000457883


  2 / 2913 MEDLINE  
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[PMID]:28154014
[Au] Autor:Kaltenmeier CT; Vollmer LL; Vernetti LA; Caprio L; Davis K; Korotchenko VN; Day BW; Tsang M; Hulkower KI; Lotze MT; Vogt A
[Ad] Endereço:Departments of Surgery, Immunology and Biochemistry (C.T.K., M.T.L.), Drug Discovery Institute (L.L.V., L.A.V., L.C., K.D., M.T.L., A.V.), Department of Computational and Systems Biology (L.A.V., A.V.), Department of Pharmaceutical Sciences (V.N.K., B.W.D.), and Department of Developmental Biology (
[Ti] Título:A Tumor Cell-Selective Inhibitor of Mitogen-Activated Protein Kinase Phosphatases Sensitizes Breast Cancer Cells to Lymphokine-Activated Killer Cell Activity.
[So] Source:J Pharmacol Exp Ther;361(1):39-50, 2017 Apr.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dual specificity mitogen-activated protein kinase (MAPK) phosphatases [dual specificity phosphatase/MAP kinase phosphatase (DUSP-MKP)] have been hypothesized to maintain cancer cell survival by buffering excessive MAPK signaling caused by upstream activating oncogenic products. A large and diverse body of literature suggests that genetic depletion of DUSP-MKPs can reduce tumorigenicity, suggesting that hyperactivating MAPK signaling by DUSP-MKP inhibitors could be a novel strategy to selectively affect the transformed phenotype. Through in vivo structure-activity relationship studies in transgenic zebrafish we recently identified a hyperactivator of fibroblast growth factor signaling [(E)-2-benzylidene-5-bromo-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one (BCI-215)] that is devoid of developmental toxicity and restores defective MAPK activity caused by overexpression of DUSP1 and DUSP6 in mammalian cells. Here, we hypothesized that BCI-215 could selectively affect survival of transformed cells. In MDA-MB-231 human breast cancer cells, BCI-215 inhibited cell motility, caused apoptosis but not primary necrosis, and sensitized cells to lymphokine-activated killer cell activity. Mechanistically, BCI-215 induced rapid and sustained phosphorylation of extracellular signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK) in the absence of reactive oxygen species, and its toxicity was partially rescued by inhibition of p38 but not JNK or ERK. BCI-215 also hyperactivated MKK4/SEK1, suggesting activation of stress responses. Kinase phosphorylation profiling documented BCI-215 selectively activated MAPKs and their downstream substrates, but not receptor tyrosine kinases, SRC family kinases, AKT, mTOR, or DNA damage pathways. Our findings support the hypothesis that BCI-215 causes selective cancer cell cytotoxicity in part through non-redox-mediated activation of MAPK signaling, and the findings also identify an intersection with immune cell killing that is worthy of further exploration.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Inibidores Enzimáticos/farmacologia
Células Matadoras Ativadas por Linfocina/efeitos dos fármacos
Células Matadoras Ativadas por Linfocina/metabolismo
Fosfatases da Proteína Quinase Ativada por Mitógeno/antagonistas & inibidores
Fosfatases da Proteína Quinase Ativada por Mitógeno/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
Neoplasias da Mama/tratamento farmacológico
Neoplasias da Mama/imunologia
Relação Dose-Resposta a Droga
Inibidores Enzimáticos/uso terapêutico
Feminino
Células HeLa
Hepatócitos/efeitos dos fármacos
Hepatócitos/imunologia
Hepatócitos/metabolismo
Seres Humanos
Proteínas Quinases JNK Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases JNK Ativadas por Mitógeno/imunologia
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Células Matadoras Ativadas por Linfocina/imunologia
Fosfatases da Proteína Quinase Ativada por Mitógeno/imunologia
Ratos
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Enzyme Inhibitors); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases); EC 3.1.3.16 (Mitogen-Activated Protein Kinase Phosphatases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.116.239756


  3 / 2913 MEDLINE  
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[PMID]:27436446
[Au] Autor:Mie K; Shimada T; Akiyoshi H; Hayashi A; Ohashi F
[Ad] Endereço:Laboratory of Veterinary Surgery, Graduate School of Life and Environmental Sciences, Osaka Prefecture University, 1-58 Rinku-oraikita, Izumisano, Osaka, 598-8531, Japan.
[Ti] Título:Change in peripheral blood lymphocyte count in dogs following adoptive immunotherapy using lymphokine-activated T killer cells combined with palliative tumor resection.
[So] Source:Vet Immunol Immunopathol;177:58-63, 2016 Sep.
[Is] ISSN:1873-2534
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We evaluated changes in peripheral blood lymphocyte (PBL) count in dogs following adoptive immunotherapy using lymphokine-activated T killer cells (T-LAK) in combination with surgery. Fifteen tumor-bearing dogs treated with T-LAK therapy combined with palliative resection of tumors were enrolled in the present study. T-LAK were generated from autologous peripheral blood mononuclear cells (PBMC) by culture with recombinant human interleukin -2 (rhIL-2) and solid phase anti-canine cluster of differentiation (CD)3 antibody. T-LAK were administrated intravenously at 2-4-week intervals. After the first administration of T-LAK, counts of PBL and T lymphocyte subsets (CD3(+), CD4(+) and CD8(+) cells) increased and the CD4/CD8 ratio decreased, with significant increases in CD8(+) cells (P<0.05). In 8 tumor-bearing dogs that were administered sequential T-LAK, available data on changes in PBL and T lymphocyte phenotypes until the fifth administration were also analyzed. In tumor-bearing dogs administered 5 rounds of T-LAK, CD8(+) cell counts were maintained high until the fifth administration of T-LAK. Moreover, the CD4/CD8 ratio remained low until the fifth administration of T-LAK. These results indicate that T-LAK therapy combined with surgery may increase peripheral blood T lymphocytes, particularly CD8(+) cells, in tumor-bearing dogs.
[Mh] Termos MeSH primário: Imunoterapia Adotiva/veterinária
Células Matadoras Ativadas por Linfocina/imunologia
Neoplasias/veterinária
[Mh] Termos MeSH secundário: Animais
Terapia Combinada/veterinária
Cães
Feminino
Seres Humanos
Imunoterapia Adotiva/métodos
Contagem de Linfócitos
Masculino
Neoplasias/imunologia
Neoplasias/terapia
Cuidados Paliativos
Subpopulações de Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170410
[Lr] Data última revisão:
170410
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160721
[St] Status:MEDLINE


  4 / 2913 MEDLINE  
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[PMID]:27127137
[Au] Autor:Yamaguchi Y; Katata Y; Okawaki M; Sawaki A; Yamamura M
[Ad] Endereço:Department of Clinical Oncology, Kawasaki Medical School and Hospital, Kurashiki, Okayama, Japan shogo@med.kawasaki-m.ac.jp.
[Ti] Título:A Prospective Observational Study of Adoptive Immunotherapy for Cancer Using Zoledronate-Activated Killer (ZAK) Cells - An Analysis for Patients with Incurable Pancreatic Cancer.
[So] Source:Anticancer Res;36(5):2307-13, 2016 May.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: Adoptive immunotherapy (AIT) using autologous zoledronate-activated killer (ZAK) cells has been performed for developing a novel modality of cancer treatment. In this study, data series from incurable pancreatic cancer were analyzed. PATIENTS AND METHODS: Patients were treated with AIT using intravenous administration of ZAK cells every 3 to 4 weeks in combination with standard chemotherapy and possible clinical benefits were examined. RESULTS: Seventy-five patients were treated. A median overall survival (OS) time of 6.7 months was achieved for all patients and 13.1 months for those treated 5 times or more, that increased to 14.6 and 18.3 months, respectively, when the previous treatment period of chemotherapy alone was included in the analysis. The disease control rate was 58.5 %. Multivariate regression analysis showed a significant positive correlation between the survival and baseline value of lymphocyte percentage in white blood cell counts (p=0.031). CONCLUSION: The data suggest that AIT using ZAK cells in combination with chemotherapy is safe and feasible and may be effective in prolonging survival for patients with incurable pancreatic cancer. The lymphocyte percentage at baseline may be a good biomarker for predicting the survival benefit of ZAK cell AIT.
[Mh] Termos MeSH primário: Difosfonatos/farmacologia
Imidazóis/farmacologia
Imunoterapia Adotiva
Células Matadoras Ativadas por Linfocina/imunologia
Neoplasias Pancreáticas/terapia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Células Cultivadas
Terapia Combinada
Desoxicitidina/administração & dosagem
Desoxicitidina/análogos & derivados
Combinação de Medicamentos
Feminino
Seres Humanos
Interleucina-2/farmacologia
Estimativa de Kaplan-Meier
Células Matadoras Ativadas por Linfocina/efeitos dos fármacos
Células Matadoras Ativadas por Linfocina/transplante
Masculino
Meia-Idade
Ácido Oxônico/administração & dosagem
Neoplasias Pancreáticas/tratamento farmacológico
Estudos Prospectivos
Terapia de Salvação
Tegafur/administração & dosagem
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Diphosphonates); 0 (Drug Combinations); 0 (Imidazoles); 0 (Interleukin-2); 0W860991D6 (Deoxycytidine); 150863-82-4 (S 1 (combination)); 1548R74NSZ (Tegafur); 5VT6420TIG (Oxonic Acid); 6XC1PAD3KF (zoledronic acid); B76N6SBZ8R (gemcitabine)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170131
[Lr] Data última revisão:
170131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160430
[St] Status:MEDLINE


  5 / 2913 MEDLINE  
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[PMID]:26902929
[Au] Autor:Ritter C; Fan K; Paulson KG; Nghiem P; Schrama D; Becker JC
[Ad] Endereço:Translational Skin Cancer Research, German Cancer Consortium (DKTK), University Hospital Essen, Germany.
[Ti] Título:Reversal of epigenetic silencing of MHC class I chain-related protein A and B improves immune recognition of Merkel cell carcinoma.
[So] Source:Sci Rep;6:21678, 2016 Feb 23.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Merkel cell carcinoma (MCC) is a virally associated cancer characterized by its aggressive behavior and strong immunogenicity. Both viral infection and malignant transformation induce expression of MHC class I chain-related protein (MIC) A and B, which signal stress to cells of the immune system via Natural Killer group 2D (NKG2D) resulting in elimination of target cells. However, despite transformation and the continued presence of virally-encoded proteins, MICs are only expressed in a minority of MCC tumors in situ and are completely absent on MCC cell lines in vitro. This lack of MIC expression was due to epigenetic silencing via MIC promoter hypo-acetylation; indeed, MIC expression was re-induced by pharmacological inhibition of histone deacetylases (HDACs) both in vitro and in vivo. This re-induction of MICs rendered MCC cells more sensitive to immune-mediated lysis. Thus, epigenetic silencing of MICs is an important immune escape mechanism of MCCs.
[Mh] Termos MeSH primário: Carcinoma de Célula de Merkel/genética
Inativação Gênica/imunologia
Antígenos de Histocompatibilidade Classe I/genética
Histona Desacetilases/genética
Células Matadoras Ativadas por Linfocina/imunologia
Neoplasias Cutâneas/genética
[Mh] Termos MeSH secundário: Acetilação/efeitos dos fármacos
Animais
Carcinoma de Célula de Merkel/tratamento farmacológico
Carcinoma de Célula de Merkel/imunologia
Carcinoma de Célula de Merkel/patologia
Linhagem Celular Tumoral
Citotoxicidade Imunológica
Inativação Gênica/efeitos dos fármacos
Antígenos de Histocompatibilidade Classe I/imunologia
Inibidores de Histona Desacetilases/farmacologia
Histona Desacetilases/imunologia
Histonas/genética
Histonas/imunologia
Seres Humanos
Ácidos Hidroxâmicos/farmacologia
Células Matadoras Ativadas por Linfocina/citologia
Células Matadoras Ativadas por Linfocina/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos NOD
Subfamília K de Receptores Semelhantes a Lectina de Células NK/genética
Subfamília K de Receptores Semelhantes a Lectina de Células NK/imunologia
Plicamicina/análogos & derivados
Plicamicina/farmacologia
Regiões Promotoras Genéticas/efeitos dos fármacos
Transdução de Sinais
Neoplasias Cutâneas/tratamento farmacológico
Neoplasias Cutâneas/imunologia
Neoplasias Cutâneas/patologia
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Histocompatibility Antigens Class I); 0 (Histone Deacetylase Inhibitors); 0 (Histones); 0 (Hydroxamic Acids); 0 (KLRK1 protein, human); 0 (MHC class I-related chain A); 0 (MICB antigen); 0 (NK Cell Lectin-Like Receptor Subfamily K); 58IFB293JI (vorinostat); 97666-60-9 (mithramycin A); EC 3.5.1.98 (Histone Deacetylases); NIJ123W41V (Plicamycin)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170408
[Lr] Data última revisão:
170408
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160224
[St] Status:MEDLINE
[do] DOI:10.1038/srep21678


  6 / 2913 MEDLINE  
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[PMID]:26727638
[Au] Autor:Mie K; Tomihari M; Hoshi K; Nakamura T; Yamaguchi T; Miyahara K; Shimada T
[Ad] Endereço:Department of Clinical Veterinary Science, Obihiro University of Agriculture and Veterinary Medicine, Nish 2-sen 11 Inada-cho, Obihiro, Hokkaido 080-8555, Japan.
[Ti] Título:Influence of transfusion of lymphokine-activated T killer cells on inflammatory responses in dogs after laparotomy.
[So] Source:J Vet Med Sci;78(4):579-85, 2016 May 03.
[Is] ISSN:1347-7439
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The influence of transfusion of lymphokine-activated T killer cells (T-LAK) on inflammatory responses was examined in dogs after laparotomy. Plasma C-reactive protein (CRP) level, cell numbers of peripheral blood lymphocytes (PBLs) and T lymphocyte subsets (CD3(+), CD4(+) and CD8(+)) and mRNA expression levels of cytokines including interleukin (IL)-2, IL-12, IL-4, IL-10 and transforming growth factor (TGF)-ß in peripheral blood mononuclear cells (PBMCs) were measured in dogs with (T-LAK group) or without (control group) a single T-LAK administration immediately after laparotomy. The plasma CRP level initially increased and then decreased to the normal range at 7 days after laparotomy in the T-LAK group, which was earlier than in the control group. The expression level of IL-10 mRNA showed a marked postoperative increase and was significantly higher than the preoperative level on day 7 (P<0.05), whereas the level in the control group showed no clear change after laparotomy. A significant increase in IL-2 mRNA expression level in the T-LAK group was observed on day 14, which was two weeks earlier than in the control group (P<0.05). These results suggest that T-LAK therapy in dogs after laparotomy leads to earlier resolution of postoperative inflammation by production of an anti-inflammatory cytokine (IL-10) in the early phase of the postoperative period and earlier restoration of cell-mediated immunity related to cytokine production by PBMCs.
[Mh] Termos MeSH primário: Inflamação/virologia
Células Matadoras Ativadas por Linfocina/transplante
Células T Matadoras Naturais/transplante
Complicações Pós-Operatórias/veterinária
[Mh] Termos MeSH secundário: Animais
Proteína C-Reativa/metabolismo
Cães
Inflamação/terapia
Interleucinas/metabolismo
Laparotomia/veterinária
Masculino
Neutrófilos/imunologia
Complicações Pós-Operatórias/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukins); 9007-41-4 (C-Reactive Protein)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160105
[St] Status:MEDLINE
[do] DOI:10.1292/jvms.15-0626


  7 / 2913 MEDLINE  
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[PMID]:26659089
[Au] Autor:García-Muñoz R; López-Díaz-de-Cerio A; Feliu J; Panizo A; Giraldo P; Rodríguez-Calvillo M; Grande C; Pena E; Olave M; Panizo C; Inogés S
[Ad] Endereço:Department of Hematology, San Pedro Hospital, Logroño, La Rioja, Spain.
[Ti] Título:Follicular lymphoma: in vitro effects of combining lymphokine-activated killer (LAK) cell-induced cytotoxicity and rituximab- and obinutuzumab-dependent cellular cytotoxicity (ADCC) activity.
[So] Source:Immunol Res;64(2):548-57, 2016 Apr.
[Is] ISSN:1559-0755
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Follicular lymphoma (FL) is a disease of paradoxes-incurable but with a long natural history. We hypothesized that a combination of lymphokine-activated killer (LAK) cells and monoclonal antibodies might provide a robust synergistic treatment and tested this hypothesis in a phase II clinical trial (NCT01329354). In this trial, in addition to R-CHOP, we alternated the administration of only rituximab with rituximab and autologous LAK cells that were expanded ex vivo. Our objective was to determine the in vitro capability of LAK cells generated from FL patients to produce cytotoxicity against tumor cell lines and to determine rituximab- and obinutuzumab-induced cytotoxicity via antibody-dependent cellular cytotoxicity (ADCC) activity. We analyzed the LAK cell-induced cytotoxicity and rituximab (R)- and obinutuzumab (GA101)-induced ADCC activity. We show that LAK cells generated from FL patients induce cytotoxicity against tumor cell lines. R and GA101 enhance cytolysis through ADCC activity of LAK cells. Impaired LAK cell cytotoxicity and ADCC activity were detected in 50 % of patients. Percentage of NK cells in LAK infusions were correlated with the R- and GA101-induced ADCC. Our results indicate that the combination of R or GA101 and LAK cells should be an option as frontline maintenance therapy in patients with FL.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/imunologia
Citotoxicidade Celular Dependente de Anticorpos/imunologia
Citotoxicidade Imunológica/imunologia
Células Matadoras Ativadas por Linfocina/imunologia
Linfoma Folicular/imunologia
Rituximab/imunologia
[Mh] Termos MeSH secundário: Anticorpos Monoclonais Humanizados/farmacologia
Antineoplásicos/farmacologia
Linhagem Celular Tumoral
Seres Humanos
Células Matadoras Ativadas por Linfocina/metabolismo
Contagem de Linfócitos
Linfoma Folicular/diagnóstico
Linfoma Folicular/tratamento farmacológico
Linfoma Folicular/metabolismo
Fenótipo
Rituximab/farmacologia
Subpopulações de Linfócitos T/imunologia
Subpopulações de Linfócitos T/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Antineoplastic Agents); 4F4X42SYQ6 (Rituximab); O43472U9X8 (obinutuzumab)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151215
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1007/s12026-015-8747-9


  8 / 2913 MEDLINE  
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[PMID]:26616436
[Au] Autor:Ishiguro M; Okada A; Asai K; Kojima K; Okada H
[Ad] Endereço:Choju Medical Institute, Fukushimura Hospital.
[Ti] Título:Stimulation of neuronal cells by culture supernatant of T lymphocytes triggered by anti-CD3 mAb followed by propagation in the presence of interleukin-2.
[So] Source:Microbiol Immunol;60(1):47-55, 2016 Jan.
[Is] ISSN:1348-0421
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Performance status (PS) frequently improves occurs in cancer patients who have been infused with their own lymphokine-activated killer T cells (LAK-T). In the present study, a culture supernatant of LAK-T (LAK-T sup) administered to 8-week-old rats caused neurogenesis as evidenced by increased 5-ethynyl-2'-deoxyuridine staining of brain tissues. Intravenous injection of granulocyte-macrophage colony stimulating factor (GM-CSF), a major cytokine in LAK-T sup, had a similar effect. Furthermore, LAK-T sup induced Ca(++) increase in rat hippocampal brain slices that was detected in neuronal cells by emission of Fluo-8 NW at 520 nm. The same effect was observed with an rGM-CSF solution. GM-CSF may activate neuronal cells by stimulating the glial cells that surround and attach to them. If so, GM-CSF and LAK-T sup may improve the motor neurons of patients with amyotrophic lateral sclerosis. The neurogenerative effect of GM-CSF in LAK-T sup may also help improve brain function in aged adults including those with dementia such as Alzheimer's disease.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/farmacologia
Interleucina-2/farmacologia
Células Matadoras Ativadas por Linfocina/imunologia
Neurônios/imunologia
Linfócitos T Citotóxicos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adulto
Doença de Alzheimer/terapia
Esclerose Amiotrófica Lateral/terapia
Animais
Encéfalo/efeitos dos fármacos
Encéfalo/imunologia
Encéfalo/patologia
Proliferação Celular/fisiologia
Citocinas/imunologia
Citometria de Fluxo
Fator Estimulador de Colônias de Granulócitos e Macrófagos/farmacologia
Seres Humanos
Imunoterapia Adotiva/métodos
Interleucina-2/imunologia
Células Matadoras Ativadas por Linfocina/citologia
Células Matadoras Ativadas por Linfocina/efeitos dos fármacos
Células Matadoras Ativadas por Linfocina/transplante
Masculino
Neurogênese/imunologia
Neurônios/citologia
Neurônios/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Ratos Wistar
Linfócitos T Citotóxicos/imunologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Cytokines); 0 (Interleukin-2); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151201
[St] Status:MEDLINE
[do] DOI:10.1111/1348-0421.12346


  9 / 2913 MEDLINE  
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[PMID]:26513172
[Au] Autor:Schellhorn M; Haustein M; Frank M; Linnebacher M; Hinz B
[Ad] Endereço:Institute of Toxicology and Pharmacology, Rostock University Medical Center, Rostock, Germany.
[Ti] Título:Celecoxib increases lung cancer cell lysis by lymphokine-activated killer cells via upregulation of ICAM-1.
[So] Source:Oncotarget;6(36):39342-56, 2015 Nov 17.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The antitumorigenic mechanism of the selective cyclooxygenase-2 (COX-2) inhibitor celecoxib is still a matter of debate. Using lung cancer cell lines (A549, H460) and metastatic cells derived from a lung cancer patient, the present study investigates the impact of celecoxib on the expression of intercellular adhesion molecule 1 (ICAM-1) and cancer cell lysis by lymphokine-activated killer (LAK) cells. Celecoxib, but not other structurally related selective COX-2 inhibitors (i.e., etoricoxib, rofecoxib, valdecoxib), was found to cause a substantial upregulation of ICAM-1 protein levels. Likewise, ICAM-1 mRNA expression was increased by celecoxib. Celecoxib enhanced the susceptibility of cancer cells to be lysed by LAK cells with the respective effect being reversed by a neutralizing ICAM-1 antibody. In addition, enhanced killing of celecoxib-treated cancer cells was reversed by preincubation of LAK cells with an antibody to lymphocyte function associated antigen 1 (LFA-1), suggesting intercellular ICAM-1/LFA-1 crosslink as crucial event within this process. Finally, celecoxib elicited no significant increase of LAK cell-mediated lysis of non-tumor bronchial epithelial cells, BEAS-2B, associated with a far less ICAM-1 induction as compared to cancer cells. Altogether, our data demonstrate celecoxib-induced upregulation of ICAM-1 on lung cancer cells to be responsible for intercellular ICAM-1/LFA-1 crosslink that confers increased cancer cell lysis by LAK cells. These findings provide proof for a novel antitumorigenic mechanism of celecoxib.
[Mh] Termos MeSH primário: Celecoxib/farmacologia
Inibidores de Ciclo-Oxigenase 2/farmacologia
Molécula 1 de Adesão Intercelular/metabolismo
Células Matadoras Ativadas por Linfocina/metabolismo
Neoplasias Pulmonares/tratamento farmacológico
Neoplasias Pulmonares/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Seres Humanos
Molécula 1 de Adesão Intercelular/imunologia
Células Matadoras Ativadas por Linfocina/imunologia
Neoplasias Pulmonares/imunologia
Transfecção
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cyclooxygenase 2 Inhibitors); 0 (ICAM1 protein, human); 126547-89-5 (Intercellular Adhesion Molecule-1); JCX84Q7J1L (Celecoxib)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151030
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.5745


  10 / 2913 MEDLINE  
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[PMID]:26276724
[Au] Autor:Fernández L; Valentín J; Zalacain M; Leung W; Patiño-García A; Pérez-Martínez A
[Ad] Endereço:Clinical Research Department, Spanish National Cancer Research Centre CNIO, C/Melchor Fernández Almagro, 3, 28029 Madrid, Spain.
[Ti] Título:Activated and expanded natural killer cells target osteosarcoma tumor initiating cells in an NKG2D-NKG2DL dependent manner.
[So] Source:Cancer Lett;368(1):54-63, 2015 Nov 01.
[Is] ISSN:1872-7980
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Current therapies fail to cure most metastatic or recurrent bone cancer. We explored the efficacy and the pathways involved in natural killer (NK) cells' elimination of osteosarcoma (OS) cells, including tumor initiating cells (TICs), which are responsible for chemotherapy resistance, recurrence, and metastasis. The expression of ligands for NK cell receptors was studied in primary OS cell lines by flow cytometry. In vitro cytotoxicity of activated and expanded NK (NKAE) cells against OS was tested, and the pathways involved explored by using specific antibody blockade. NKAE cells' ability to target OS TICs was analyzed by flow cytometry and sphere formation assays. Spironolactone (SPIR) was tested for its ability to increase OS cells' susceptibility to NK cell lysis in vitro and in vivo. We found OS cells were susceptible to NKAE cells' lysis both in vivo and in vitro, and this cytolytic activity relied on interaction between NKG2D receptor and NKG2D ligands (NKG2DL). SPIR increased OS cells' susceptibility to lysis by NKAE cells, and could shrink the OS TICs. Our results show NKAE cells target OS cells including the TICs compartment, supporting the use of NK-cell based immunotherapies for OS.
[Mh] Termos MeSH primário: Neoplasias Ósseas/terapia
Proliferação Celular
Imunoterapia Adotiva/métodos
Células Matadoras Ativadas por Linfocina/transplante
Ativação Linfocitária
Subfamília K de Receptores Semelhantes a Lectina de Células NK/metabolismo
Células-Tronco Neoplásicas/metabolismo
Osteossarcoma/terapia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Neoplasias Ósseas/imunologia
Neoplasias Ósseas/metabolismo
Neoplasias Ósseas/patologia
Comunicação Celular
Linhagem Celular Tumoral
Técnicas de Cocultura
Citotoxicidade Imunológica
Seres Humanos
Células Matadoras Ativadas por Linfocina/imunologia
Células Matadoras Ativadas por Linfocina/metabolismo
Ligantes
Camundongos Endogâmicos NOD
Camundongos SCID
Subfamília K de Receptores Semelhantes a Lectina de Células NK/imunologia
Células-Tronco Neoplásicas/efeitos dos fármacos
Células-Tronco Neoplásicas/imunologia
Células-Tronco Neoplásicas/patologia
Osteossarcoma/imunologia
Osteossarcoma/metabolismo
Osteossarcoma/patologia
Transdução de Sinais
Espironolactona/farmacologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (KLRK1 protein, human); 0 (Ligands); 0 (NK Cell Lectin-Like Receptor Subfamily K); 27O7W4T232 (Spironolactone)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:150831
[Lr] Data última revisão:
150831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150816
[St] Status:MEDLINE



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