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  1 / 2268 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


  2 / 2268 MEDLINE  
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[PMID]:29277767
[Au] Autor:Gao Y; Barmada MA; Bergman I
[Ad] Endereço:Department of Pediatrics, Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, PA, U.S.A.
[Ti] Título:Antitumor Memory T-Cells Become Functionally Mature from 30 to 100 days in a Mouse Model of Neoplasia.
[So] Source:Anticancer Res;38(1):147-157, 2018 01.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Late metastases develop from cancer of the breast, prostate, lung, kidney and malignant melanomas. Memory T-cells have excellent potential to prevent this devastating development in the same way that they routinely prevent emergence of latent viruses. MATERIAL AND METHODS: A peritoneal tumor mouse model of viral oncotherapy was used to generate therapeutic antitumor memory T-cells. Functional in vivo and in vitro assays were used to study the temporal evolution of their anticancer effects. RESULTS: Highly therapeutic antitumor memory was generated by viral oncolytic immunotherapy 30 days after treatment and matured to maximal potency at 100 days. Maturation was not uniform across different measures. CONCLUSION: The results provide guidelines for developing a viral oncolytic vaccine strategy to generate antitumor memory T-cells that can eliminate small nests of metastatic cancer cells in sanctuary sites and prevent emergence of tumors from dormant cancer cell collections. The results are relevant to any immunization strategy designed to generate antitumor memory T-cells.
[Mh] Termos MeSH primário: Imunoterapia
Terapia Viral Oncolítica
Neoplasias Peritoneais/terapia
Linfócitos T/citologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Modelos Animais de Doenças
Feminino
Camundongos Endogâmicos BALB C
Neoplasias Peritoneais/imunologia
Vesiculovirus
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE


  3 / 2268 MEDLINE  
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[PMID]:28929492
[Au] Autor:Li Y; Hong J; Oh JE; Yoon AR; Yun CO
[Ad] Endereço:Graduate Program for Nanomedical Science, Yonsei University, Seoul, Korea.
[Ti] Título:Potent antitumor effect of tumor microenvironment-targeted oncolytic adenovirus against desmoplastic pancreatic cancer.
[So] Source:Int J Cancer;142(2):392-413, 2018 Jan 15.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pancreatic cancer is a leading cause of cancer-related death. Desmoplastic pancreatic tumors exhibit excessive extracellular matrix (ECM) and are thus highly resistant to anticancer therapeutics, since the ECM restricts drug penetration and dispersion. Here, we designed and generated two hypoxia-responsive and cancer-specific hybrid promoters, H(mT)E and H(E)mT. Transgene expression driven by each hybrid promoter was markedly higher under hypoxic conditions than normoxic conditions. Moreover, H(E)mT-driven transgene expression was highly cancer-specific and was superior to that of H(mT)E-driven expression. A decorin-expressing oncolytic adenovirus (Ad; oH(E)mT-DCN) replicating under the control of the H(E)mT promoter induced more potent and highly cancer-specific cell death compared with its cognate control oncolytic Ad, which harbored the endogenous Ad E1A promoter. Moreover, oH(E)mT-DCN exhibited enhanced antitumor efficacy compared with both the clinically approved oncolytic Ad ONYX-015 and its cognate control oncolytic Ad lacking DCN. oH(E)mT-DCN treatment also attenuated the expression of major ECM components, such as collagen I/III, elastin and fibronectin and induced tumor cell apoptosis, leading to extensive viral dispersion within orthotopic pancreatic tumors and pancreatic cancer patient-derived tumor spheroids. Collectively, these findings demonstrate that oH(E)mT-DCN exhibits potent antitumor efficacy by degrading the ECM and inducing apoptosis in a multifunctional process. This process facilitates the dispersion and replication of oncolytic Ad, making it an attractive candidate for the treatment of aggressive and desmoplastic pancreatic cancer.
[Mh] Termos MeSH primário: Adenoviridae/genética
Terapia Viral Oncolítica
Neoplasias Pancreáticas/terapia
Microambiente Tumoral
[Mh] Termos MeSH secundário: Animais
Apoptose
Proliferação Celular
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Masculino
Camundongos
Camundongos Nus
Neoplasias Pancreáticas/genética
Neoplasias Pancreáticas/patologia
Células Tumorais Cultivadas
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171214
[Lr] Data última revisão:
171214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.31060


  4 / 2268 MEDLINE  
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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 / 2268 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]:28886381
[Au] Autor:Ribas A; Dummer R; Puzanov I; VanderWalde A; Andtbacka RHI; Michielin O; Olszanski AJ; Malvehy J; Cebon J; Fernandez E; Kirkwood JM; Gajewski TF; Chen L; Gorski KS; Anderson AA; Diede SJ; Lassman ME; Gansert J; Hodi FS; Long GV
[Ad] Endereço:University of California at Los Angeles, Jonsson Comprehensive Cancer Center, Los Angeles, CA, USA. Electronic address: aribas@mednet.ucla.edu.
[Ti] Título:Oncolytic Virotherapy Promotes Intratumoral T Cell Infiltration and Improves Anti-PD-1 Immunotherapy.
[So] Source:Cell;170(6):1109-1119.e10, 2017 Sep 07.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Here we report a phase 1b clinical trial testing the impact of oncolytic virotherapy with talimogene laherparepvec on cytotoxic T cell infiltration and therapeutic efficacy of the anti-PD-1 antibody pembrolizumab. Twenty-one patients with advanced melanoma were treated with talimogene laherparepvec followed by combination therapy with pembrolizumab. Therapy was generally well tolerated, with fatigue, fevers, and chills as the most common adverse events. No dose-limiting toxicities occurred. Confirmed objective response rate was 62%, with a complete response rate of 33% per immune-related response criteria. Patients who responded to combination therapy had increased CD8 T cells, elevated PD-L1 protein expression, as well as IFN-γ gene expression on several cell subsets in tumors after talimogene laherparepvec treatment. Response to combination therapy did not appear to be associated with baseline CD8 T cell infiltration or baseline IFN-γ signature. These findings suggest that oncolytic virotherapy may improve the efficacy of anti-PD-1 therapy by changing the tumor microenvironment. VIDEO ABSTRACT.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/administração & dosagem
Melanoma/terapia
Terapia Viral Oncolítica/efeitos adversos
[Mh] Termos MeSH secundário: Terapia Combinada
Herpesviridae/genética
Seres Humanos
Imunoterapia
Receptor de Morte Celular Programada 1/antagonistas & inibidores
Microambiente Tumoral
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (PDCD1 protein, human); 0 (Programmed Cell Death 1 Receptor); DPT0O3T46P (pembrolizumab)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


  7 / 2268 MEDLINE  
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[PMID]:28874392
[Au] Autor:Zhu Z; Gorman MJ; McKenzie LD; Chai JN; Hubert CG; Prager BC; Fernandez E; Richner JM; Zhang R; Shan C; Tycksen E; Wang X; Shi PY; Diamond MS; Rich JN; Chheda MG
[Ad] Endereço:Department of Medicine, Division of Regenerative Medicine, University of California, San Diego, School of Medicine, La Jolla, CA.
[Ti] Título:Zika virus has oncolytic activity against glioblastoma stem cells.
[So] Source:J Exp Med;214(10):2843-2857, 2017 Oct 02.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glioblastoma is a highly lethal brain cancer that frequently recurs in proximity to the original resection cavity. We explored the use of oncolytic virus therapy against glioblastoma with Zika virus (ZIKV), a flavivirus that induces cell death and differentiation of neural precursor cells in the developing fetus. ZIKV preferentially infected and killed glioblastoma stem cells (GSCs) relative to differentiated tumor progeny or normal neuronal cells. The effects against GSCs were not a general property of neurotropic flaviviruses, as West Nile virus indiscriminately killed both tumor and normal neural cells. ZIKV potently depleted patient-derived GSCs grown in culture and in organoids. Moreover, mice with glioblastoma survived substantially longer and at greater rates when the tumor was inoculated with a mouse-adapted strain of ZIKV. Our results suggest that ZIKV is an oncolytic virus that can preferentially target GSCs; thus, genetically modified strains that further optimize safety could have therapeutic efficacy for adult glioblastoma patients.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/virologia
Glioblastoma/virologia
Células-Tronco Neoplásicas/virologia
Terapia Viral Oncolítica/métodos
Zika virus/fisiologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos Alquilantes/uso terapêutico
Neoplasias Encefálicas/terapia
Linhagem Celular Tumoral
Proliferação Celular
Cercopithecus aethiops
Terapia Combinada
Dacarbazina/análogos & derivados
Dacarbazina/uso terapêutico
Feminino
Imunofluorescência
Glioblastoma/terapia
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Neoplasias Experimentais/terapia
Neoplasias Experimentais/virologia
Células Vero
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Alkylating); 7GR28W0FJI (Dacarbazine); YF1K15M17Y (temozolomide)
[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:170907
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20171093


  8 / 2268 MEDLINE  
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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 / 2268 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 / 2268 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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