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  1 / 1534 MEDLINE  
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[PMID]:28460470
[Au] Autor:Cheng T; Song Y; Zhang Y; Zhang C; Yin J; Chi Y; Zhou D
[Ad] Endereço:Vaccine Research Center, Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Science, Shanghai 200031, China.
[Ti] Título:A novel oncolytic adenovirus based on simian adenovirus serotype 24.
[So] Source:Oncotarget;8(16):26871-26885, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Among the oncolytic virotherapy, an emerging treatment for tumor, adenoviruses are widely used at present in preclinical and clinical trials. Traditionally, oncolytic adenoviruses were developed based on the human adenovirus serotype 5 (AdHu5). However, AdHu5 has the drawbacks of preexisting anti-AdHu5 immunity in most populations, and extensive sequestration of Adhu5 by the liver through hexon, blood coagulation factor X (FX), and FX receptor interactions. To tackle these problems, we explored a novel oncolytic adenovirus AdC7-SP/E1A-ΔE3 for cancer treatment. AdC7-SP/E1A-ΔE3 was constructed by replacing the E1A promoter with tumor specific promoter survivin promoter and deleting E3 region using direct cloning methods based on simian adenovirus serotype 24 (namely AdC7). We showed that AdC7-SP/E1A-ΔE3 significantly killed tumor cell lines NCI-H508 and Huh7, and inhibited tumor growth in both NCI-H508 and Huh7 xenograft tumor models. Importantly, AdC7-SP/E1A-ΔE3 exhibited the antitumor efficacy via systemic administration. Mechanistically, infected cells were killed by AdC7-SP/E1A-ΔE3 via the p53-independent mitochondrial apoptosis pathway in which phosphorylation of BAD markedly declined and the expresses of Bik significantly went up. Therefore, AdC7-SP/E1A-ΔE3 is a promising candidate for liver and colon tumor treatment.
[Mh] Termos MeSH primário: Adenovirus dos Símios/classificação
Adenovirus dos Símios/genética
Vetores Genéticos/genética
Vírus Oncolíticos/genética
[Mh] Termos MeSH secundário: Proteínas E1A de Adenovirus/genética
Animais
Apoptose/genética
Linhagem Celular Tumoral
Efeito Citopatogênico Viral
Modelos Animais de Doenças
Deleção de Genes
Expressão Gênica
Engenharia Genética
Terapia Genética
Vetores Genéticos/administração & dosagem
Vetores Genéticos/efeitos adversos
Seres Humanos
Proteínas Inibidoras de Apoptose/genética
Camundongos
Mitocôndrias/genética
Terapia Viral Oncolítica
Especificidade de Órgãos/genética
Regiões Promotoras Genéticas
Sorogrupo
Transdução de Sinais
Carga Tumoral
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
Replicação Viral
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adenovirus E1A Proteins); 0 (BIRC5 protein, human); 0 (Inhibitor of Apoptosis Proteins); 0 (Tumor Suppressor Protein p53)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15845


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[PMID]:28982603
[Au] Autor:Rush BS; Coughlin ML; Sanyal G
[Ad] Endereço:Analytical Sciences, Biopharmaceutical Development, MedImmune LLC, One MedImmune Way, Gaithersburg, MD 20878, United States.
[Ti] Título:In vitro infectivity of oncolytic Newcastle Disease Virus: Correlation between plaque and fluorescent focus assays.
[So] Source:J Virol Methods;251:69-74, 2018 Jan.
[Is] ISSN:1879-0984
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Newcastle Disease Virus (NDV) is an avian paramyxovirus that has no significant pathogenicity in humans. Cancer cells with impaired immune defense mechanisms are susceptible to infection and lysis by NDV. A recombinant construct of a lentogenic form of NDV (rNDV) containing an insertion of granulocyte macrophage colony stimulating factor (GMCSF) transgene was earlier reported and shown to have acceptably low avian pathogenicity as well as oncolytic potential. Reliable measurement of infectious titer is key to determining the effectiveness of virus preparations to infect and lyse cells. We report here a comparative evaluation of two infectious titer assays as applied to rNDV: plaque assay and fluorescent focus assay (FFA). Optimization of assay conditions for both titer methods has produced concordant results spanning several orders of magnitude. While plaque formation is the gold standard measure of virus titer, FFA provides higher throughput and faster turn-around. FFA has been further evaluated on two different instrument platforms, for automated versus manual foci recognition and counting, with equivalent results. These results point to amenability of FFA to transfer between different laboratories and analysts, without introducing significant subjectivity in data analysis.
[Mh] Termos MeSH primário: Vírus da Doença de Newcastle/crescimento & desenvolvimento
Vírus Oncolíticos/crescimento & desenvolvimento
Imagem Óptica/métodos
Carga Viral/métodos
Ensaio de Placa Viral/métodos
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:COMPARATIVE STUDY; EVALUATION STUDIES; JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171007
[St] Status:MEDLINE


  3 / 1534 MEDLINE  
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[PMID]:28466296
[Au] Autor:Suryawanashi YR; Zhang T; Woyczesczyk HM; Christie J; Byers E; Kohler S; Eversole R; Mackenzie C; Essani K
[Ad] Endereço:Laboratory of Virology, Department of Biological Sciences, Western Michigan University, Kalamazoo, MI, 49008-5410, USA.
[Ti] Título:T-independent response mediated by oncolytic tanapoxvirus recombinants expressing interleukin-2 and monocyte chemoattractant protein-1 suppresses human triple negative breast tumors.
[So] Source:Med Oncol;34(6):112, 2017 Jun.
[Is] ISSN:1559-131X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human triple negative breast cancer (TNBC) is an aggressive disease, associated with a high rate of recurrence and metastasis. Current therapeutics for TNBC are limited, highly toxic and show inconsistent efficacy due to a high degree of intra-tumoral and inter-tumoral heterogeneity. Oncolytic viruses (OVs) are an emerging treatment option for cancers. Several OVs are currently under investigation in preclinical and clinical settings. Here, we examine the oncolytic potential of two tanapoxvirus (TPV) recombinants expressing mouse monocyte chemoattractant protein (mMCP)-1 [also known as mCCL2] and mouse interleukin (mIL)-2, in human TNBC, in vitro and in vivo. Both wild-type (wt) TPV and TPV recombinants demonstrated efficient replicability in human TNBC cells and killed cancer cell efficiently in a dose-dependent manner in vitro. TPV/∆66R/mCCL2 and TPV/∆66R/mIL-2 expressing mCCL2 and mIL-2, respectively, suppressed the growth of MDA-MB-231 tumor xenografts in nude mice significantly, as compared to the mock-injected tumors. Histological analysis of tumors showed areas of viable tumor cells, necrotic foci and immune cell accumulation in virus-treated tumors. Moreover, TPV/∆66R/mIL-2-treated tumors showed a deep infiltration of mononuclear immune cells into the tumor capsule and focal cell death in tumors. In conclusion, TPV recombinants expressing mCCL2 and mIL-2 showed a significant therapeutic effect in MDA-MB-231 tumor xenografts, in nude mice through induction of potent antitumor immune responses. Considering the oncolytic potency of armed oncolytic TPV recombinants expressing mCCL2 and mIL-2 in an experimental nude mouse model, these viruses merit further investigation as alternative treatment options for human breast cancer.
[Mh] Termos MeSH primário: Quimiocina CCL2/metabolismo
Imunoterapia/métodos
Interleucina-2/metabolismo
Vírus Oncolíticos/genética
Neoplasias de Mama Triplo Negativas/metabolismo
Yatapoxvirus/genética
[Mh] Termos MeSH secundário: Animais
Aotidae
Linhagem Celular
Quimiocina CCL2/genética
Quimiocina CCL2/imunologia
Seres Humanos
Interleucina-2/genética
Interleucina-2/imunologia
Masculino
Camundongos
Camundongos Nus
Vírus Oncolíticos/metabolismo
Neoplasias de Mama Triplo Negativas/genética
Neoplasias de Mama Triplo Negativas/imunologia
Ensaios Antitumorais Modelo de Xenoenxerto
Yatapoxvirus/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CCL2); 0 (Interleukin-2)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180111
[Lr] Data última revisão:
180111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1007/s12032-017-0973-7


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[PMID]:27776794
[Au] Autor:Hock K; Laengle J; Kuznetsova I; Egorov A; Hegedus B; Dome B; Wekerle T; Sachet M; Bergmann M
[Ad] Endereço:Department of Surgery, Medical University of Vienna, Vienna, Austria.
[Ti] Título:Oncolytic influenza A virus expressing interleukin-15 decreases tumor growth in vivo.
[So] Source:Surgery;161(3):735-746, 2017 03.
[Is] ISSN:1532-7361
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Interleukin-15 has become a promising molecule in the context of eliciting an effective, antitumor immune response because it is able to stimulate cells of the innate and adaptive immune system. METHODS: We generated an interleukin-15-expressing oncolytic influenza A virus for the treatment of an established murine tumor model. RESULTS: Our oncolytic influenza A virus produced large amounts of interleukin-15 and induced proliferation and activation of human T cells in vitro. Intraperitoneal administration increased the amount of mouse natural killer cells and effector memory T cells, as well as T cell reactivity in vivo. Moreover, intratumoral injection induced a profound decrease in growth of established tumors in mice and increased the amount of tumor-infiltrating T cells and natural killer cells. CONCLUSION: We established a stable, IL-15-producing oncolytic influenza A virus with promising immunostimulatory and antitumor attributes.
[Mh] Termos MeSH primário: Vírus da Influenza A
Interleucina-15/fisiologia
Melanoma Experimental/patologia
Terapia Viral Oncolítica
Vírus Oncolíticos
Neoplasias Cutâneas/patologia
[Mh] Termos MeSH secundário: Animais
Técnicas de Cultura de Células
Proliferação Celular/efeitos dos fármacos
Feminino
Seres Humanos
Células Matadoras Naturais/efeitos dos fármacos
Melanoma Experimental/terapia
Camundongos
Camundongos Endogâmicos C57BL
Neoplasias Cutâneas/terapia
Linfócitos T/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-15)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171210
[Lr] Data última revisão:
171210
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161106
[St] Status:MEDLINE


  5 / 1534 MEDLINE  
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[PMID]:28988534
[Au] Autor:Zhirnov OP
[Ad] Endereço:Ivanovsky Institute of Virology, Gamaleya Microbiology and Epidemiology Research Center, Moscow, 123098, Russia. zhirnov@inbox.ru.
[Ti] Título:Biochemical Variations in Cytolytic Activity of Ortho- and Paramyxoviruses in Human Lung Tumor Cell Culture.
[So] Source:Biochemistry (Mosc);82(9):1048-1054, 2017 Sep.
[Is] ISSN:1608-3040
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human lung cancer cells (Calu-3 line) were studied for the development of apoptosis, necrosis, and autophagy in response to infection with ortho- and paramyxoviruses. Biochemical pathways underlying various mechanisms of cell death differed for different viruses. When infected with murine Sendai paramyxovirus, Calu-3 cells demonstrated typical necrotic features such as cell swelling (but not shrinkage), lack of chromatin DNA laddering, of caspase 3 and 8 activation, and of apoptotic cleavage of poly(ADP-ribose) polymerase (PARP) protein; an activation of antiapoptotic protein kinase Akt was also revealed. In contrast, infection with avian influenza virus A/FPV/Rostock/34 (H7N1 subtype) or Newcastle disease virus (NDV, avian paramyxovirus) caused the development of typical apoptotic markers such as cell shrinkage, ladder-type chromosomal DNA fragmentation, caspase 3 and 8 activation, and proteolytic cleavage of PARP in the absence of Akt activation. Notably, no upregulation of p53 protein phosphorylation was observed in all infected cells, which indicates that p53 is not involved in the virus-induced death of Calu-3 cells. Cell death caused by the influenza virus was accompanied by overstimulation of autophagy, whereas no stimulation of autophagy was observed in the NDV-infected cells. Infection with Sendai virus caused moderate stimulation of autophagy, which suggests that the mechanism of the virus-induced cell death and the balance between autophagy and cell death in infected cancer cells depend on the virus type and might significantly differ even for closely related viruses. Therefore, an optimal strategy for oncolytic virus-mediated destruction of tumor cells in cancer patients requires selection of the most appropriate oncolytic virus based on the mechanism of its cytolytic action in a particular type of tumor.
[Mh] Termos MeSH primário: Apoptose
Vírus da Influenza A Subtipo H7N1
Neoplasias Pulmonares/virologia
Vírus da Doença de Newcastle
Vírus Oncolíticos
Vírus Sendai
[Mh] Termos MeSH secundário: Autofagia
Seres Humanos
Neoplasias Pulmonares/patologia
Necrose
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171010
[St] Status:MEDLINE
[do] DOI:10.1134/S0006297917090085


  6 / 1534 MEDLINE  
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[PMID]:28934210
[Au] Autor:Mahasa KJ; Eladdadi A; de Pillis L; Ouifki R
[Ad] Endereço:DST/NRF Centre of Excellence in Epidemiological Modelling and Analysis (SACEMA), University of Stellenbosch, Stellenbosch, South Africa.
[Ti] Título:Oncolytic potency and reduced virus tumor-specificity in oncolytic virotherapy. A mathematical modelling approach.
[So] Source:PLoS One;12(9):e0184347, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the present paper, we address by means of mathematical modeling the following main question: How can oncolytic virus infection of some normal cells in the vicinity of tumor cells enhance oncolytic virotherapy? We formulate a mathematical model describing the interactions between the oncolytic virus, the tumor cells, the normal cells, and the antitumoral and antiviral immune responses. The model consists of a system of delay differential equations with one (discrete) delay. We derive the model's basic reproductive number within tumor and normal cell populations and use their ratio as a metric for virus tumor-specificity. Numerical simulations are performed for different values of the basic reproduction numbers and their ratios to investigate potential trade-offs between tumor reduction and normal cells losses. A fundamental feature unravelled by the model simulations is its great sensitivity to parameters that account for most variation in the early or late stages of oncolytic virotherapy. From a clinical point of view, our findings indicate that designing an oncolytic virus that is not 100% tumor-specific can increase virus particles, which in turn, can further infect tumor cells. Moreover, our findings indicate that when infected tissues can be regenerated, oncolytic viral infection of normal cells could improve cancer treatment.
[Mh] Termos MeSH primário: Neoplasias/terapia
Terapia Viral Oncolítica
Vírus Oncolíticos/fisiologia
[Mh] Termos MeSH secundário: Algoritmos
Simulação por Computador
Seres Humanos
Modelos Biológicos
Neoplasias/imunologia
Neoplasias/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184347


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[PMID]:28922411
[Au] Autor:Zhao X; Ouyang W; Chester C; Long S; Wang N; He Z
[Ad] Endereço:Stem Cell and Tissue Engineering Research Center, Guizhou Medical University, Guiyang, Guizhou, China.
[Ti] Título:Cytokine-induced killer cell delivery enhances the antitumor activity of oncolytic reovirus.
[So] Source:PLoS One;12(9):e0184816, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oncolytic viruses (OV) have recently emerged as a promising therapeutic modality in cancer treatment. OV selectively infect and kill tumor cells, while sparing untransformed cells. The direct cytotoxic effects combined with the capacity to trigger an immune response make OV an appealing combination partner in the burgeoning field of cancer immunotherapy. One of the leading OV therapeutic candidates is the double-stranded RNA virus reovirus. In order to improve the oncolytic activity of reovirus and allow for systemic administration despite the prevalence of neutralizing antibodies, cytokine-induced killer (CIK) cells were explored as cell carriers for reovirus delivery. In this study, CIK cells were successfully loaded with reovirus ex vivo, and viral replication was limited in CIK cells. Confocal microscopy and flow cytometry demonstrated that CIK cells retained reovirus on the surface. Moreover, CIK cells could promote reovirus infection of tumor cells in the presence of neutralizing antibodies; meanwhile, cytotoxicity of CIK cells was increased after loading with reovirus. These findings support further investigation of reovirus and CIK combination for antitumor therapy.
[Mh] Termos MeSH primário: Células Matadoras Induzidas por Citocinas/imunologia
Imunidade Celular
Orthoreovirus Mamífero 3/fisiologia
Neoplasias/imunologia
Neoplasias/terapia
Vírus Oncolíticos/fisiologia
Replicação Viral/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Seres Humanos
Camundongos
Neoplasias/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184816


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[PMID]:28857157
[Au] Autor:Schwaiger T; Knittler MR; Grund C; Roemer-Oberdoerfer A; Kapp JF; Lerch MM; Mettenleiter TC; Mayerle J; Blohm U
[Ad] Endereço:Institute of Immunology, Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health, Greifswald-Insel Riems, Germany.
[Ti] Título:Newcastle disease virus mediates pancreatic tumor rejection via NK cell activation and prevents cancer relapse by prompting adaptive immunity.
[So] Source:Int J Cancer;141(12):2505-2516, 2017 Dec 15.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pancreatic cancer is the 8th most common cause of cancer-related deaths worldwide and the tumor with the poorest prognosis of all solid malignancies. In 1957, it was discovered that Newcastle disease virus (NDV) has oncolytic properties on tumor cells. To study the oncolytic properties of NDV in pancreatic cancer a single dose was administered intravenously in a syngeneic orthotopic tumor model using two different murine pancreatic adenocarcinoma cell lines (DT6606PDA, Panc02). Tumor growth was monitored and immune response was analyzed. A single treatment with NDV inhibited DT6606PDA tumor growth in mice and prevented recurrence for a period of three months. Tumor infiltration and systemic activation of NK cells, cytotoxic and helper T-cells was enhanced. NDV-induced melting of Panc02 tumors until d7 pi, but they recurred displaying unrestricted tumor growth, low immunogenicity and inhibition of tumor-specific immune response. Arrest of DT6606PDA tumor growth and rejection was mediated by activation of NK cells and a specific antitumor immune response via T-cells. Panc02 tumors rapidly decreased until d7 pi, but henceforth tumors characterized by the ability to perform immune-regulatory functions reappeared. Our results demonstrated that NDV-activated immune cells are able to reject tumors provided that an adaptive antitumor immune response can be initiated. However, activated NK cells that are abundant in Panc02 tumors lead to outgrowth of nonimmunogenic tumor cells with inhibitory properties. Our study emphasizes the importance of an adaptive immune response, which is initiated by NDV to mediate long-term tumor surveillance in addition to direct oncolysis.
[Mh] Termos MeSH primário: Imunidade Adaptativa
Recidiva Local de Neoplasia/prevenção & controle
Vírus da Doença de Newcastle/imunologia
Vírus Oncolíticos/imunologia
Neoplasias Pancreáticas/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Seres Humanos
Células Matadoras Naturais/metabolismo
Ativação Linfocitária
Camundongos
Terapia Viral Oncolítica
Neoplasias Pancreáticas/patologia
Linfócitos T Auxiliares-Indutores/metabolismo
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.31026


  9 / 1534 MEDLINE  
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[PMID]:28810147
[Au] Autor:Saha D; Martuza RL; Rabkin SD
[Ad] Endereço:Molecular Neurosurgery Laboratory and the Brain Tumor Research Center, Department of Neurosurgery, Massachusetts General Hospital, Boston, MA, USA; Department of Neurosurgery, Harvard Medical School, Boston, MA, USA.
[Ti] Título:Macrophage Polarization Contributes to Glioblastoma Eradication by Combination Immunovirotherapy and Immune Checkpoint Blockade.
[So] Source:Cancer Cell;32(2):253-267.e5, 2017 Aug 14.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glioblastoma is an immunosuppressive, fatal brain cancer that contains glioblastoma stem-like cells (GSCs). Oncolytic herpes simplex virus (oHSV) selectively replicates in cancer cells while inducing anti-tumor immunity. oHSV G47Δ expressing murine IL-12 (G47Δ-mIL12), antibodies to immune checkpoints (CTLA-4, PD-1, PD-L1), or dual combinations modestly extended survival of a mouse glioma model. However, the triple combination of anti-CTLA-4, anti-PD-1, and G47Δ-mIL12 cured most mice in two glioma models. This treatment was associated with macrophage influx and M1-like polarization, along with increased T effector to T regulatory cell ratios. Immune cell depletion studies demonstrated that CD4 and CD8 T cells as well as macrophages are required for synergistic curative activity. This combination should be translatable to the clinic and other immunosuppressive cancers.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/uso terapêutico
Antígeno CTLA-4/antagonistas & inibidores
Glioblastoma/terapia
Imunoterapia
Interleucina-12/genética
Macrófagos/imunologia
Terapia Viral Oncolítica
Receptor de Morte Celular Programada 1/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Antígeno B7-H1/antagonistas & inibidores
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/metabolismo
Linfócitos T CD4-Positivos/patologia
Linfócitos T CD8-Positivos/imunologia
Linfócitos T CD8-Positivos/metabolismo
Linfócitos T CD8-Positivos/patologia
Pontos de Checagem do Ciclo Celular/efeitos dos fármacos
Terapia Combinada
Modelos Animais de Doenças
Feminino
Glioblastoma/imunologia
Seres Humanos
Ativação de Macrófagos
Macrófagos/metabolismo
Macrófagos/patologia
Camundongos
Camundongos Endogâmicos C57BL
Vírus Oncolíticos/genética
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (B7-H1 Antigen); 0 (CD274 protein, human); 0 (CTLA-4 Antigen); 0 (CTLA4 protein, human); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor); 187348-17-0 (Interleukin-12)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE


  10 / 1534 MEDLINE  
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[PMID]:28810141
[Au] Autor:Bell JC; Ilkow CS
[Ad] Endereço:Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada; Ottawa Hospital Research Institute, 501 Smyth Road, Ottawa, ON K1H 8L6, Canada. Electronic address: jbell@ohri.ca.
[Ti] Título:A Viro-Immunotherapy Triple Play for the Treatment of Glioblastoma.
[So] Source:Cancer Cell;32(2):133-134, 2017 08 14.
[Is] ISSN:1878-3686
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this issue of Cancer Cell, Saha et al. systematically test and optimize combination therapy strategies in a challenging model of glioblastoma. Durable complete responses were seen only when an oncolytic virus expressing IL12 was coupled with anti-CTLA-4 and anti-PD-1 therapeutics.
[Mh] Termos MeSH primário: Glioblastoma
Imunoterapia
[Mh] Termos MeSH secundário: Terapia Combinada
Seres Humanos
Terapia Viral Oncolítica
Vírus Oncolíticos
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE



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