Relevant bibliographies by topics / Oncolytic viru

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
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Academic literature on the topic 'Oncolytic viru'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Oncolytic viru"

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Shin, Dong Ho, Teresa Nguyen, Bulent Ozpolat, Frederick Lang, Marta Alonso, Candelaria Gomez-Manzano, and Juan Fueyo. "Current strategies to circumvent the antiviral immunity to optimize cancer virotherapy." Journal for ImmunoTherapy of Cancer 9, no. 4 (April 2021): e002086. http://dx.doi.org/10.1136/jitc-2020-002086.

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Cancer virotherapy is a paradigm-shifting treatment modality based on virus-mediated oncolysis and subsequent antitumor immune responses. Clinical trials of currently available virotherapies showed that robust antitumor immunity characterizes the remarkable and long-term responses observed in a subset of patients. These data suggest that future therapies should incorporate strategies to maximize the immunotherapeutic potential of oncolytic viruses. In this review, we highlight the recent evidence that the antiviral immunity of the patients may limit the immunotherapeutic potential of oncolytic viruses and summarize the most relevant approaches to strategically redirect the immune response away from the viruses and toward tumors to heighten the clinical impact of viro-immunotherapy platforms.
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Raimondi, Giulia, Sabrina Gea-Sorlí, Marc Otero-Mateo, and Cristina Fillat. "Inhibition of miR-222 by Oncolytic Adenovirus-Encoded miRNA Sponges Promotes Viral Oncolysis and Elicits Antitumor Effects in Pancreatic Cancer Models." Cancers 13, no. 13 (June 28, 2021): 3233. http://dx.doi.org/10.3390/cancers13133233.

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Oncolytic adenoviruses (OA) are envisioned as a therapeutic option for patients with cancer, designed to preferentially replicate in cancer cells. However, the high number of genetic alterations in tumors can generate a context in which adenoviruses have difficulties replicating. Abnormal miRNAs expression is a trademark of pancreatic cancer, with several oncogenic miRNAs playing essential roles in cancer-associated pathways. The perturbed miRNome induces reprogramming of gene expression in host cells that can impact the complex interplay between cellular processes and viral replication. We have studied the effects of overexpressed miRNAs on oncolytic adenoviral activity and identified miRNAs modulators of adenoviral oncolysis in pancreatic cancer cells. Inhibition of the highly upregulated miR-222 sensitized cancer cells to oncolysis. To provide a therapeutic application to this insight, we engineered the oncolytic adenovirus AdNuPARmE1A with miR-222 binding sites, working as sponges to withdraw the miRNA from the cellular environment. AdNuPAR-E-miR222-S mediated-decrease of miR-222 expression in pancreatic cancer cells strongly improved the viral yield and enhanced the adenoviral cytotoxic effects. Antitumoral studies confirmed a high activity for AdNuPARmE1A-miR222-S in vivo, controlling tumor progression more effectively than the scrambled control virus in xenografts. We demonstrated that the increased antitumor potency of the novel oncolytic virus resulted from the combinatory effects of miR-222 oncomiR inhibition and the restoration of miR-222 target genes activity enhancing viral fitness.
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Nguyen, Duong Hoang, Thomas Herrmann, Barbara Härtl, Dobrin Draganov, Ivelina Minev, Forrest Neuharth, Alberto Gomez, et al. "Development of Allogeneic Stem Cell-Based Platform for Delivery and Potentiation of Oncolytic Virotherapy." Cancers 14, no. 24 (December 13, 2022): 6136. http://dx.doi.org/10.3390/cancers14246136.

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We describe the repurposing and optimization of the TK-positive (thymidine kinase) vaccinia virus strain ACAM1000/ACAM2000™ as an oncolytic virus. This virus strain has been widely used as a smallpox vaccine and was also used safely in our recent clinical trial in patients with advanced solid tumors and Acute Myeloid Leukemia (AML). The vaccinia virus was amplified in CV1 cells and named CAL1. CAL1 induced remarkable oncolysis in various human and mouse cancer cells and preferentially amplified in cancer cells, supporting the use of this strain as an oncolytic virus. However, the therapeutic potential of CAL1, as demonstrated with other oncolytic viruses, is severely restricted by the patients’ immune system. Thus, to develop a clinically relevant oncolytic virotherapy agent, we generated a new off-the-shelf therapeutic called Supernova1 (SNV1) by loading CAL1 virus into allogeneic adipose-derived mesenchymal stem cells (AD-MSC). Culturing the CAL1-infected stem cells allows the expression of virally encoded proteins and viral amplification prior to cryopreservation. We found that the CAL1 virus loaded into AD-MSC was resistant to humoral inactivation. Importantly, the virus-loaded stem cells (SNV1) released larger number of infectious viral particles and virally encoded proteins, leading to augmented therapeutic efficacy in vitro and in animal tumor models.
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Petrov, Ivan, Ivaylo Gentschev, Anna Vyalkova, Mohamed I. Elashry, Michele C. Klymiuk, Stefan Arnhold, and Aladar A. Szalay. "Canine Adipose-Derived Mesenchymal Stem Cells (cAdMSCs) as a “Trojan Horse” in Vaccinia Virus Mediated Oncolytic Therapy against Canine Soft Tissue Sarcomas." Viruses 12, no. 7 (July 12, 2020): 750. http://dx.doi.org/10.3390/v12070750.

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Several oncolytic viruses (OVs) including various human and canine adenoviruses, canine distemper virus, herpes-simplex virus, reovirus, and members of the poxvirus family, such as vaccinia virus and myxoma virus, have been successfully tested for canine cancer therapy in preclinical and clinical settings. The success of the cancer virotherapy is dependent on the ability of oncolytic viruses to overcome the attacks of the host immune system, to preferentially infect and lyse cancer cells, and to initiate tumor-specific immunity. To date, several different strategies have been developed to overcome the antiviral host defense barriers. In our study, we used canine adipose-derived mesenchymal stem cells (cAdMSCs) as a “Trojan horse” for the delivery of oncolytic vaccinia virus Copenhagen strain to achieve maximum oncolysis against canine soft tissue sarcoma (CSTS) tumors. A single systemic administration of vaccinia virus-loaded cAdMSCs was found to be safe and led to the significant reduction and substantial inhibition of tumor growth in a CSTS xenograft mouse model. This is the first example that vaccinia virus-loaded cAdMSCs could serve as a therapeutic agent against CSTS tumors.
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Woo, Yanghee, Susanne G. Warner, Rula Geha, Marianne M. Stanford, Penelope Decarolis, Masmudur M. Rahman, Samuel Singer, Grant McFadden, and Yuman Fong. "The Oncolytic Activity of Myxoma Virus against Soft Tissue Sarcoma Is Mediated by the Overexpression of Ribonucleotide Reductase." Clinical Medicine Insights: Oncology 15 (January 2021): 117955492199306. http://dx.doi.org/10.1177/1179554921993069.

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Background: Myxoma virus (MYXV) is an oncolytic poxvirus that lacks the gene for 1 of the subunits of ribonucleotide reductase (RR), a crucial DNA synthesis and repair enzyme. The overexpression of RR has been implicated in the invasiveness of several cancers, including soft tissue sarcomas (STS). The purpose of the study was to investigate the oncolytic efficacy of MYXV in STS with different levels of RR expression. Methods: The oncolytic effect of recombinant MYXV was evaluated in 4 human STS cell lines, LS141 (a dedifferentiated liposarcoma), DDLS8817 (a dedifferentiated liposarcoma), RDD2213 (recurrent dedifferentiated liposarcoma), and HSSYII (a synovial sarcoma) using infectivity and cytotoxicity assays. Following the overexpression of RRM2 by cDNA transfection and silencing of RRM2 by siRRM2 in these STS cell lines, the RRM2 expression levels were analyzed by Western blot. Results: We observed a direct correlation between viral oncolysis and RRM2 mRNA levels ( R = 0.96) in STS. Higher RRM2 expression was associated with a more robust cell kill. Silencing the RRM2 gene led to significantly greater cell survival (80%) compared with the control group ( P = .003), whereas overexpression of the RRM2 increased viral oncolysis by 33% ( P < .001). Conclusions: Our results show that the oncolytic effects of MYXV correlate directly with RR expression levels and are enhanced in STS cell lines with naturally occurring or artificially induced high expression levels of RR. Myxoma virus holds promise in the treatment of advanced soft tissue cancer, especially in tumors overexpressing RR.
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Martikainen, Miika, and Magnus Essand. "Virus-Based Immunotherapy of Glioblastoma." Cancers 11, no. 2 (February 5, 2019): 186. http://dx.doi.org/10.3390/cancers11020186.

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Glioblastoma (GBM) is the most common type of primary brain tumor in adults. Despite recent advances in cancer therapy, including the breakthrough of immunotherapy, the prognosis of GBM patients remains dismal. One of the new promising ways to therapeutically tackle the immunosuppressive GBM microenvironment is the use of engineered viruses that kill tumor cells via direct oncolysis and via stimulation of antitumor immune responses. In this review, we focus on recently published results of phase I/II clinical trials with different oncolytic viruses and the new interesting findings in preclinical models. From syngeneic preclinical GBM models, it seems evident that oncolytic virus-mediated destruction of GBM tissue coupled with strong adjuvant effect, provided by the robust stimulation of innate antiviral immune responses and adaptive anti-tumor T cell responses, can be harnessed as potent immunotherapy against GBM. Although clinical testing of oncolytic viruses against GBM is at an early stage, the promising results from these trials give hope for the effective treatment of GBM in the near future.
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Ekeke, Chigozirim N., Kira L. Russell, Kyla Joubert, David L. Bartlett, James D. Luketich, Adam C. Soloff, Zong Sheng Guo, Michael T. Lotze, and Rajeev Dhupar. "Fighting Fire With Fire: Oncolytic Virotherapy for Thoracic Malignancies." Annals of Surgical Oncology 28, no. 5 (February 11, 2021): 2715–27. http://dx.doi.org/10.1245/s10434-020-09477-4.

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AbstractThoracic malignancies are associated with high mortality rates. Conventional therapy for many of the patients with thoracic malignancies is obviated by a high incidence of locoregional recurrence and distant metastasis. Fortunately, developments in immunotherapy provide effective strategies for both local and systemic treatments that have rapidly advanced during the last decade. One promising approach to cancer immunotherapy is to use oncolytic viruses, which have the advantages of relatively high tumor specificity, selective replication-mediated oncolysis, enhanced antigen presentation, and potential for delivery of immunogenic payloads such as cytokines, with subsequent elicitation of effective antitumor immunity. Several oncolytic viruses including adenovirus, coxsackievirus B3, herpes virus, measles virus, reovirus, and vaccinia virus have been developed and applied to thoracic cancers in preclinical murine studies and clinical trials. This review discusses the current state of oncolytic virotherapy in lung cancer, esophageal cancer, and metastatic malignant pleural effusions and considers its potential as an emergent therapeutic for these patients.
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Chavez, Valery A., Floritza Bustamante, Abner Murray, Ashok Saluja, and Jaime Merchan. "Abstract 96: A novel virus-drug combination to enhance oncolysis in colorectal cancer (crc)." Cancer Research 82, no. 12_Supplement (June 15, 2022): 96. http://dx.doi.org/10.1158/1538-7445.am2022-96.

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Abstract Background: While advances in immune and targeted therapies improve outcomes in selected cancers, only a minority of colorectal cancer (CRC) patients benefit from them. Oncolytic viruses (OVs) represent novel cancer biotherapies, and among them, the oncolytic measles virus (MV) has demonstrated safety and antitumor activity in early clinical studies. MV alone does is not associated with cancer cures. Triptolide, a diterpenoid epoxide extracted from the thunder god vine (Tripterygium wilfordii), has been reported to have potent antitumor effects via multiple mechanisms, including anti-proliferative, pro-apoptotic, antiangiogenic, and induction of ER stress. The effects of triptolide on viral colon cancer oncolysis have not been previously investigated. Objectives: To characterize the in vitro and in vivo mechanisms of novel stromal retargeted oncolytic MVs and improve efficacy by combining MVs with triptolide. Methods: The in vitro effects of triptolide alone, MV-GFP (Edmonston strain of Measles virus expressing eGFP, for human cancer cells), MV-m-uPA (MV retargeted against the murine uPA receptor, for murine cancer cells), or virus-triptolide combinations on tumor cell cytotoxicity were assessed by cell count (Vi cell counter) or xCelligence assays, on HT-29, HCT116, SW620, CT26, and MC38 cells. Molecular and mechanistic characterization of Triptolide’s effects alone and combination with MV in HT29 cells will be analyzed by the (Reverse Phase Protein Array (RPPA) and validated by western blot analysis (experiment undergoing). In vivo effects (tumor progression and survival) of minnelide (M) (water-soluble version of Triptolide) alone and in combination with Measles Virus were assessed in Balb/C mice bearing CT26. Results: While MV and T had dose-dependent cytotoxic activity as single agents, significant augmentation of MV oncolysis was induced by co-treatment with triptolide. In vivo experiments showed similar effects observed in vitro, with potent antitumor activity of triptolide and enhanced in vivo antitumor activity when minnelide was combined with MV vectors. Conclusions: our results strongly suggest that triptolide or minnelide enhances measles virus oncolysis in vitro and in vivo models of colorectal cancer. In vitro and in vivo mechanistic studies are underway to characterize the molecular mechanisms by which triptolide enhances MV oncolysis and will be presented at the meeting. Citation Format: Valery A. Chavez, Floritza Bustamante, Abner Murray, Ashok Saluja, Jaime Merchan. A novel virus-drug combination to enhance oncolysis in colorectal cancer (crc) [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 96.
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Wang, Guan. "Immunodominant and cryptic tumor neoantigen-specific immune responses activated by an armed oncolytic virus expressing a PD-L1 inhibitor." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 136.5. http://dx.doi.org/10.4049/jimmunol.202.supp.136.5.

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Abstract Tumor neoantigens are exclusively expressed in malignant cells representing an ideal target for tumor immunotherapy. Oncolytic virus selectively infects and lyses tumor cells releasing a full-array tumor antigens and danger factors. Combined with PD1 checkpoint blockade, oncolytic virus triggered tumor neoantigen-specific T cell immune responses through local treatments. The present study developed a novel therapeutic regimen that combines ddVV, GM-CSF, and a PD-L1 inhibitor into a single therapeutic agent by engineering ddVV to co-express GM-CSF and a PD-L1 inhibitor. The novel therapeutic regimen has triple functions: ddVV-mediated oncolysis, GM-CSF-mediated enhancement of dendritic cell recruitment and function, and PD-L1 inhibitor-mediated interruption of PD-1/PD-L1 interaction. As a result, the double-armed oncolytic virus eradicated primary tumor and prevented tumor recurrence more efficiently after local administration. Analyses of underlying mechanisms revealed that the double-armed ddVV possessed a superior capability of improving tumor environment and triggering systemic T cell immune responses against not only dominant but also cryptic tumor neo-antigens in tumor mouse models.
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Sherwood, Matthew, Robert Ewing, Carolini Kaid, Thiago Giove Mitsugi, and Keith Okamoto. "MOMC-1. Employing the Zika Virus to kill paediatric nervous system tumour cells." Neuro-Oncology Advances 3, Supplement_2 (July 1, 2021): ii3. http://dx.doi.org/10.1093/noajnl/vdab070.011.

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Abstract Malignant paediatric nervous system tumours, such as Medulloblastoma, Neuroblastoma and ATRT commonly harbour tumour cells with stem-like features which are highly tumorigenic and resistant to conventional cancer therapies. These tumours can exhibit high lethality and may result in severe sequelae, including cognitive and motor deficits that significantly affect patients’ quality of life. Oncolytic virotherapy is a novel therapy class that exploits viruses that preferentially infect and destroy tumour cells. These viruses present a unique advantage in targeting highly heterogeneous cancers, such as nervous system tumours, as they possess a secondary mechanism of action through which they induce a tumour-specific immune response. Clinical studies employing oncolytic virotherapy have in general reported low toxicity and minimal adverse effects, deeming oncolytic virotherapy as a potentially attractive and safer intervention against paediatric tumours. The Zika virus (ZIKV) is capable of infecting and destroying neural stem-like cancer cells from human embryonal Central Nervous System (CNS) tumours in vitro and in vivo. Infection of CNS tumour cells with ZIKV effectively inhibits tumour metastasis in mice and, in some cases, induces complete tumour remission. Neuroblastoma arises from immature nerve cells and multiple Neuroblastoma cell lines are susceptible to ZIKV infection and oncolysis. These initial findings have demonstrated the potential for a ZIKV-based virotherapy against paediatric nervous system tumours and warrants examination into the molecular mechanisms through which ZIKV executes its oncolytic ability. My research goal is to elucidate the mechanisms which are of paramount importance for ZIKV-induced oncolysis of brain tumour and Neuroblastoma cells. Utilising global expression omics profiling of ZIKV infection and mapping of viral protein-host protein interactions will identify these mechanisms both at the cellular pathway and molecular levels. These collectively will inform our understanding of how we can employ a future ZIKV-based virotherapy against paediatric nervous system tumours.
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Dissertations / Theses on the topic "Oncolytic viru"

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FROECHLICH, GUENDALINA. "DISSECTING THE STING-DEPENDENT MOLECULAR MECHANISMS IN A PRECLINICAL MODEL OF COMBINED TREATMENT WITH TUMOUR-TARGETED HERPES SIMPLEX VIRUS AND IMMUNE CHECKPOINT BLOCKADE." Doctoral thesis, Università degli Studi di Milano, 2021. http://hdl.handle.net/2434/883382.

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Oncolytic viruses promote anti-tumour immune response by direct tumour cell killing and activation of intratumoural immune system. The role of innate antiviral immune response to oncolytic viruses is still debated, as they counteract viral replication and trigger adaptive antitumor immunity. The DNA sensing-mediated cGAS/STING axis may act as a key balancer between lytic and immunotherapeutic activity of oncolytic viruses. Indeed, upon infection, viral DNA is sensed by cGAS/STING axis that, in turn, induces type-I interferon cascade counteracting viral replication and spread. For this reason, STING represents a hurdle for classical lytic-centric function of oncolytic viruses. On the other side, the immunological role of STING should also be considered, as it is emerging as a key bridge between innate and adaptive immunity. To evaluate the role of STING expression in tumour cells in response to onco-virotherapy, we generated murine STING KO tumour cell lines through CRISPR/Cas9 genome editing. Preclinical studies in syngeneic immunocompetent tumour-bearing mice showed that the inactivation of STING in tumour cells, while favouring oncolytic viral replication, impaired the immunotherapeutic effects of combination therapy based on herpetic oncolytic virus and PD1 blockade. Molecular characterization of tumours revealed that loss of STING prevents antitumour immune activation inducing a tolerogenic cell death and immunosuppressive tumour microenvironment. Accordingly, I propose that antiviral, tumourresident STING provides fundamental contributions to heat-up the TME eliciting immunotherapeutic efficacy of oncolytic viruses.
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Komar, Monica. "Potentiating the Oncolytic Efficacy of Poxviruses." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23114.

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Several wild-type poxviruses have emerged as potential oncolytic viruses (OVs), including orf virus (OrfV), and vaccinia virus (VV). Oncolytic VVs have been modified to include attenuating mutations that enhance their tumour selective nature, but these mutations also reduce overall viral fitness in cancer cells. Previous studies have shown that a VV (Western Reserve) with its E3L gene replaced with the E3L homologue from, OrfV (designated VV-E3LOrfV), maintained its ability to infect cells in vitro, but was attenuated compared to its parental VV in vivo. Our goal was to determine the safety and oncolytic potential VV-E3LOrfV, compared to wild type VV and other attenuated recombinants. VV-E3LOrfV, was unable to replicate to the same titers and was sensitive to IFN compared to its parental virus and other attenuated VVs in normal human fibroblast cells. The virus was also less pathogenic when administered in vivo. Viral replication, spread and cell killing, as measures of oncolytic potential in vitro, along with in vivo efficacy, were also observed.. The Parapoxvirus, OrfV has been shown to have a unique immune-stimulation profile, inducing a number of pro-inflammatory cytokines, as well as potently recruiting and activating a number of immune cells. Despite this unique profile, OrfV is limited in its ability to replicate and spread in human cancer cells. Various strategies were employed to enhance the oncolytic efficacy of wild-type OrfV. A transient transfection/infection screen was created to determine if any of the VV host-range genes (C7L, K1L, E3L or K3L) would augment OrfV oncolysis. Combination therapy, including the use of microtubule targeting agents, Viral Sensitizer (VSe) compounds and the addition of soluble VV B18R gene product were employed to see if they also enhance OrfV efficacy. Unfortunately, none of the strategies mentioned were able to enhance OrfV.
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Heiber, Joshua F. "Characterization and Development of Vesicular Stomatitis Virus For Use as an Oncolytic Vector." Scholarly Repository, 2011. http://scholarlyrepository.miami.edu/oa_dissertations/600.

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Oncolytic virotherapy is emerging as a new treatment option for cancer patients. At present, there are relatively few oncolytic virus clinical trials that are underway or have been conducted, however one virus that shows promise in pre-clinical models is Vesicular Stomatitis Virus (VSV). VSV is a naturally occurring oncolytic rhabdovirus that has the ability to preferentially replicate in and kill malignant versus normal cells. VSV also has a low seroprevalence, minimal associated morbidity and mortality in humans, and simple non-integrating genome that can be genetically manipulated, making it an optimal oncolytic vector. Currently, many labs are using a variety of different strategies including inserting trans genes that can modulate the innate and adaptive immune response. VSV can also be retargeted by altering its surface glycoprotein (G) or be made replication incompetent by deleting the G protein. Currently, our lab has engineered a series of new recombinant VSVs, incorporating either the murine p53 (mp53), IPS-1, or TRIF transgene. mp53, IPS-1 and TRIF were incorporated into the normal VSV-XN2 genome and mp53 was also incorporated into the mutated VSV-ΔM vector generating VSV-mp53, VSV-IPS-1, VSV-TRIF and VSV-ΔM-mp53. Our data using these new viruses indicate that these viruses preferentially replicate in and kill transformed versus non-transformed cells and efficiently express the transgene. However, despite the ability for VSV-IPS-1 and VSV-TRIF to induce a robust type 1 IFN response, VSV-ΔM-mp53 was the only construct that had reduced toxicity and elicited an increased anti-tumor response against a syngeneic metastatic mammary tumor model. VSV- ΔM-mp53 treatment lead to a reduction in IL-6 and IP-10 production, an increase in tumor specific CD8+ T cells, and immunologic memory against the tumor. Collectively these studies highlight the necessity for additional VSV construct development and the generation of new clinically relevant treatment schema.
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Jamieson-Datzkiw, Taylor Rae. "A Tailored Viro-Immunotherapy Combination Approach for the Treatment of BRCA1/2 Mutated Breast and Ovarian Cancers." Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/42736.

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Hereditary breast and ovarian cancers (HBOC) represent 5-10% of breast and 10-15% of ovarian cancer cases. These cancers tend to be aggressive and curative treatment strategies are scarce. Poly(ADP-ribose) polymerase inhibitors (PARPi), a family of drugs that inhibit DNA repair, are a promising therapy for cancers harbouring mutations in their DNA repair machinery, such as HBOC. Unfortunately, nearly all patients ultimately become resistant to PARPi, leaving limited options for definitive treatment. Oncolytic or “cancer-killing” viruses are an innovative immunotherapeutic platform capable of selectively targeting cancer cells, leaving healthy tissues unharmed. Our group has demonstrated that oncolytic rhabdoviruses may be used to deliver therapeutic payloads by encoding targeting sequences to act on genes via RNA interference. In the present work, I have engineered the oncolytic virus, vesicular stomatitis virus (VSV), to express a variety of microRNA (miRNA) sequences that target genes essential for DNA repair, sensitizing resistant cancer cells to PARPi therapy. After initial experiments revealed hurdles concerning the functionality of artificial miRNAs which specifically target BRCA1 and BRCA2 I encoded the naturally occurring hsa-miR-182 into VSV to knockdown BRCA1 and additional genes essential for DNA repair. Using a 3D spheroid model, I have demonstrated sensitization of initially resistant MDA-MB-231 breast cancer cells to the PARPi, rucaparib. Complementary work exploring the shuttling of miRNAs into small extracellular vesicles, or EVs, has also shown that we can take advantage of the EV packaging facilities in infected cells, inducing the packaging of miRNAs over-expressed by VSV (EV-miRNAs) into EVs. Future work will address the functionality of these EV-miRNAs, testing their ability to knockdown targets in uninfected cancer cells.
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Selman, Mohammed. "Pharmacological Improvement of Oncolytic Virotherapy." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37626.

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Oncolytic viruses (OV) are an emerging class of anticancer bio-therapeutics that induce antitumor immunity through selective replication in cancer cells. However, the efficacy of OVs as single agents remains limited. We postulate that resistance to oncolytic virotherapy results in part from the failure of tumor cells to be sufficiently infected. In this study, we provide evidence that in the context of sarcoma, a highly heterogeneous malignancy, the infection of tumors by different oncolytic viruses varies greatly. Similarly, for a given oncolytic virus, productive infection of tumors across patient samples varies by many orders of magnitude. To overcome this issue, we hypothesize that the infection of resistant tumors can be achieved through the use of selected small molecules. Here, we have identified two novel drug classes with the ability to improve the efficacy of OV therapy: fumaric and maleic acid esters (FMAEs) and vanadium compounds. FMAEs are enhancing infection of cancer cells by several oncolytic viruses in cancer cell lines and human tumor biopsies. The ability of FMAEs to enhance viral spread is due to their ability to inhibit type I IFN production and response, which is associated with their ability to block nuclear translocation of transcription factor NF-κB. Vanadium-based phosphatase inhibitors enhance OV infection of RNA viruses in vitro and ex vivo, in resistant cancer cell lines. Mechanistically, this involves subverting the antiviral type I IFN response towards a death-inducing and proinflammatory type II IFN response, leading to improved OV spread, increased bystander killing of cancer cells, and enhanced anti-tumor immune-stimulation. Both FMAEs and vanadium compounds improve therapeutic outcomes of OV treatment in syngeneic tumor models, leading to durable responses, even in models otherwise refractory to OV and drug alone. Overall, we showcased novel avenues for the development of improved immunotherapy strategies.
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Muharemagic, Darija. "Aptamers as Enhancers of Oncolytic Virus Therapy." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32170.

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Oncolytic viruses promise to significantly improve current cancer treatments through their tumour-selective replication and multimodal attack against cancer cells. However, one of the biggest setbacks for oncolytic virus therapies is the intravenous delivery of the virus, as it can be cleared by neutralizing antibodies (nAbs) from the bloodstream before it reaches the tumour cells. In our group, we have succeeded in developing aptamers to vesicular stomatitis virus (VSV), as well as to rabbit anti-VSV polyclonal neutralizing antibodies (nAbs). We tested these aptamers’ biological activity with a cell-based plaque forming assay and found that the aptamers prevented in vitro neutralization of VSV by nAbs and increased the virus infection rate of transformed cells up to 77%. In line with this approach, we enhanced the delivery of oncolytic viruses by selecting aptamers to the CT26 colon carcinoma cell line. The binding of aptamer pools has been tested on flow cytometry and the best pools were subjected to high throughput sequencing. Selected aptamers were linked to anti-VSV aptamers and applied for target delivery of the virus to cancer cells. Development of this aptamer-based technology aims to improve viral anti-cancer therapies, with a potential to be applied as treatment for patients affected with cancer. Finally, in collaboration with a group from Erlangen University, we performed an aptamer selection using capillary electrophoresis and cell-SELEX. The target, the extracellular domain of human CD83, is a maturation marker for dendritic cells and is involved in the regulation of the immune system. Selected aptamer sequences bound selectively to mature dendritic cells, in comparison to immature dendritic cells, and thus hold promise to be applied for further studies leading to a better understanding of CD83’s mechanism of action.
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Lemay, Chantal. "Harnessing Oncolytic Virus-mediated Anti-tumour Immunity." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23318.

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Treatment of permissive tumours with the oncolytic virus (OV) VSV-Δ51 leads to a robust anti-tumour T cell response, which contributes to efficacy; however, many tumours are not permissive to in vivo treatment with VSV-Δ51. In an attempt to channel the immune stimulatory properties of VSV-Δ51 and broaden the scope of tumours that can be treated by an OV, a potent oncolytic vaccine platform was developed, consisting of tumour cells infected with VSV-Δ51. I demonstrate that prophylactic immunization with this infected cell vaccine (ICV) protected mice from subsequent tumour challenge, and expression of GM-CSF by the virus (VSVgm-ICV) increased efficacy. Immunization with VSVgm-ICV in the VSV-resistant B16-F10 model induced maturation of dendritic cells, natural killer (NK) cells, and T cells. I demonstrate that this approach is robust enough to control the growth of established and spontaneous tumours. This strategy is broadly applicable because of VSV’s extremely broad tropism, allowing nearly all cell types to be infected at high MOIs in vitro, where the virus replication kinetics outpace the cellular IFN response. It is also personalized to the unique tumour antigen(s) displayed by the cancer cell. Histone deacetylase inhibitors (HDIs) can augment viral replication, making them particularly interesting complements to OV therapy. However, the impact of HDIs on the generation and re-stimulation of immune responses remains to be clearly elucidated. Along with my collaborators at McMaster University, I demonstrate that MS-275, but not SAHA, selectively depletes naïve and regulatory lymphocytes. Memory lymphocytes that are being boosted remain unscathed and even have enhanced cytokine production, potentially as a consequence of the depleted lymphocyte compartment. This leads to a delay in anti-VSV neutralizing antibodies and T cell responses. Interestingly, HDI treatment of B16-F10 cells appears to inhibit VSV replication but allows for a longer persistence within the tumour. When used in an oncolytic prime/boost vaccination model, MS-275 potently enhanced survival. Though the anti-tumour immune response is enhanced, a near complete reduction in autoimmune vitiligo is observed with MS-275 administration. Therefore, this HDI uniquely modulates the immune response to enhance anti-tumour immunity and decrease the anti-viral response, while also decreasing autoimmune sequelae.
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Zeicher, Marc. "Oncolytic viruses cancer therapy." Doctoral thesis, Universite Libre de Bruxelles, 2008. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210439.

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Wild-type viruses with intrinsic oncolytic capacity in human includes DNA viruses like some autonomous parvoviruses and many RNA viruses. Recent advances in molecular biology have allowed the design of several genetically modified viruses, such as adenovirus and herpes simplex virus that specifically replicate in, and kill tumor cells. However, still several hurdles regarding clinical limitations and safety issues should be overcome before this mode of therapy can become of clinical relevance. It includes limited virus spread in tumor masses, stability of virus in the blood, trapping within the liver sinusoids, transendothelial transfer, and/or vector diffusion of viral particles to tumor cells, limited tumor transduction, immune-mediated inactivation or destruction of the virus. For replication-competent vectors without approved antiviral agents, suicide genes might be used as fail-safe mechanism. Cancer stem cells are a minor population of tumor cells that possess the stem cell property of self-renewal. Therefore, viruses that target the defective self-renewal pathways in cancer cells might lead to improved outcomes.

In this thesis, data we generated in the field of oncolytic autonomous parvoviruses are presented.

We replaced capsid genes by reporter genes and assessed expression in different types of human cancer cells and their normal counterparts, either at the level of whole cell population, (CAT ELISA) or at the single cell level, (FACS analysis of Green Fluorescent Protein). Cat expression was substantial (up to 10000 times background) in all infected tumor cells, despite variations according to the cell types. In contrast, no gene expression was detected in similarly infected normal cells, (with the exception of an expression slightly above background in fibroblasts.). FACS analysis of GFP expression revealed that most tumor cells expressed high level of GFP while no GFP positive normal cells could be detected with the exception of very few (less than 0.1%) human fibroblast cells expressing high level of GFP. We also replace capsid genes by genes coding for the costimulatory molecules B7-1 and B7-2 and show that, upon infection with B7 recombinant virions, only tumor cells display the costimulatory molecules and their immunogenicity was increased without any effect on normal cells. Using a recombinant MVM containig the Herpes Simplex thymidine kinase gene, we could get efficient killing of most tumor cell types in the presence of ganciclovir, whithout affecting normal proliferating cells. We also produced tetracycline inducible packaging cell lines in order to improve recombinant vectors yields. The prospects and limitations of these different strategies will be discussed.

An overview is given of the general mechanisms and genetic modifications by which oncolytic viruses achieve tumor cell-specific replication and antitumor efficacy. However, as their therapeutic efficacy in clinical trials is still not optimal, strategies are evaluated that could further enhance the oncolytic potential of conditionally replicating viruses in conjunction with other standard therapies.

Another exciting new area of research has been the harnessing of naturally tumor-homing cells as carrier cells to deliver oncolytic viruses to tumors. The trafficking of these tumor-homing cells (stem cells, immune cells and cancer cells), which support proliferation of the viruses, is mediated by specific chemokines and cell adhesion molecules and we are just beginning to understand the roles of these molecules. Finally, we will explore some ways deserving further study in order to be able to utilize various oncolytic viruses for effective cancer treatment.


Doctorat en sciences, Spécialisation biologie moléculaire
info:eu-repo/semantics/nonPublished

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Evgin, Laura. "Enhancing the Delivery of Oncolytic Vaccinia Virus to the Tumors of Hosts with Pre-Existing Immunity." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32423.

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Oncolytic viruses (OVs) have begun to show their promise in the clinical setting, however these results have been predominantly associated with loco-regional administration of virus. The treatment of metastatic disease necessitates a systemic approach to virus delivery. The circulatory system, though, is a hostile environment for viruses and the advantages associated with intravenous (IV) delivery come at a heavy cost that must be understood and brokered. Pre-existing immunity, specifically through the function of antibody and complement, poses a significant hurdle to the IV delivery of infectious virus to dispersed tumor beds. This is of particular importance for therapeutic vaccinia viruses as a majority of today’s cancer patients were vaccinated during the smallpox eradication campaign. In vitro neutralization assays of oncolytic vaccinia virus demonstrated that the antibodies elicited from smallpox vaccination, and also the anamnestic response in patients undergoing Pexa-Vec treatment, was minimally neutralizing in the absence of functional complement. Accordingly, in a Fischer rat model, complement depletion stabilized virus in the blood of pre-immunized hosts and correlated with improved delivery to mammary adenocarcinoma tumors. Complement depletion additionally enhanced infection of tumors following direct intratumoral injection of virus. The feasibility and safety of using a complement inhibitor, CP40, was tested in a cynomolgus macaque model. Immune animals saw an average 10-fold increase in infectious virus titer at an early point after the infusion, and a prolongation of the time during which infectious virus was still detectable in the blood. We have also demonstrated that vaccinia virus engages in promiscuous interactions with cells in the blood and that these interactions may be partially complement-dependent. Additionally, we have translated this complement inhibition approach to other OV candidates and found that reovirus, measles virus and a virus pseudo typed with the LCMV glycoprotein all elicit antibodies, that to some degree, are dependent on complement activation to neutralize their target viruses. We show here that capitalizing on the complement dependence of anti-viral antibody with adjunct complement inhibitors may increase the effective dose to enable successful delivery of multiple rounds of OV in immune hosts.
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Pelin, Adrian. "Bio-Engineering Vaccinia Viruses for Increased Oncolytic Potential." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39909.

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Vaccinia virus has a large and still incompletely understood genome although several strains of this virus are already in clinical development. For the most part, clinical candidates have been attenuated from their wild type vaccine strains through deletion of metabolic genes like the viral thymidine kinase gene. In the present work, we thoroughly examined the genetic elements of vaccinia which could be modulated to improve tailor the virus as a cancer therapeutic. Using a variety of cancer cell lines and primary tumor explants, we performed a fitness assay that directly compares multiple wild-type Vaccinia strains to identify the genetic elements that together create an optimal “oncolytic engine”. Using a transposon insertion strategy and deep sequencing of viral populations we systematically examined Vaccinia genes that do or do not play a role in the therapeutic activity of the virus. Our studies allowed us to identify a variety of genes in the vaccinia genome that when deleted, augment the oncolytic activity of a newly engineered Vaccinia virus. In the context of this thesis, I define enhanced oncolytic activity as superior therapeutic activity, increased immunogenicity and an improved safety profile, all aspects which we used to compare this novel virus to Vaccinia viruses currently in the clinic.
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Books on the topic "Oncolytic viru"

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Oncolytic Virus Immunotherapy. MDPI, 2022. http://dx.doi.org/10.3390/books978-3-0365-2548-8.

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Fournier, Philippe, and Volker Schirrmacher, eds. Harnessing Oncolytic Virus-mediated Antitumor Immunity. Frontiers SA Media, 2015. http://dx.doi.org/10.3389/978-2-88919-450-6.

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Oncoviruses and Their Inhibitors. Taylor & Francis Group, 2014.

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Book chapters on the topic "Oncolytic viru"

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Kirn, David. "Oncolytic Virus." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_4231-5.

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Kirn, David. "Oncolytic Virus." In Encyclopedia of Cancer, 3221–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_4231.

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Kirn, David. "Oncolytic Virus." In Encyclopedia of Cancer, 2629–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4231.

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Komarova, Natalia L., and Dominik Wodarz. "Spatial Oncolytic Virus Dynamics." In Targeted Cancer Treatment in Silico, 195–213. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8301-4_14.

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Monga, Varun, Seth M. Maliske, and Mohammed Milhem. "Oncolytic Virus Immunotherapy in Sarcoma." In Immunotherapy of Sarcoma, 69–116. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-93530-0_5.

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Komarova, Natalia L., and Dominik Wodarz. "Axiomatic Approaches to Oncolytic Virus Modeling." In Targeted Cancer Treatment in Silico, 171–94. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8301-4_13.

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Zommer, Henni, and Tamir Tuller. "The Potential of Computational Genomics in the Design of Oncolytic Viruses." In Virus Bioinformatics, 245–62. Boca Raton: Chapman and Hall/CRC, 2021. http://dx.doi.org/10.1201/9781003097679-12.

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Agarwalla, Pankaj K., and Manish K. Aghi. "Oncolytic Herpes Simplex Virus Engineering and Preparation." In Methods in Molecular Biology, 1–19. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-340-0_1.

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Msaouel, Pavlos, Ianko D. Iankov, Cory Allen, Stephen J. Russell, and Evanthia Galanis. "Oncolytic Measles Virus Retargeting by Ligand Display." In Methods in Molecular Biology, 141–62. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-340-0_11.

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Pan, Catherina X., Daniel Y. Kim, and Vinod E. Nambudiri. "Novel Cancer Treatment Using Oncolytic Virus Therapy." In Handbook of Cancer and Immunology, 1–43. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-80962-1_251-1.

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Conference papers on the topic "Oncolytic viru"

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Kurokawa, Cheyne, Sonia Agrawal, Abhisek Mitra, Elena Galvani, Shannon Burke, Ankita Varshine, Raymond Rothstein, et al. "835 AZD4820 oncolytic vaccinia virus encoding IL-12 mediates anti-tumor activity through oncolysis and tumor-specific immunity." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0835.

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Harper, James A., Shannon Burke, Andrew Leinster, Nicola Rath, Xing Cheng, Hong Jin, Robert W. Wilkinson, and Danielle Carroll. "Abstract 1456: MEDI5395: A recombinant oncolytic virus with oncolytic and immune modulatory properties." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1456.

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Harper, James A., Shannon Burke, Andrew Leinster, Nicola Rath, Xing Cheng, Hong Jin, Robert W. Wilkinson, and Danielle Carroll. "Abstract 1456: MEDI5395: A recombinant oncolytic virus with oncolytic and immune modulatory properties." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1456.

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Hutzler, Stefan, Stephanie Erbar, Robert A. Jabulowsky, Tim Beissert, Jan Hanauer, Oezlem Tuereci, Rita Mitnacht-Kraus, et al. "Abstract B040: Oncolytic measles virus for tumor vaccination." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-b040.

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Jung, Mi-Yeon, Matthew K. Ennis, Chetan P. Offord, and David Dingli. "Abstract 4947: Quantitativein vivoimaging of oncolytic virus replication." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-4947.

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Reese, David M. "Abstract IA24: New frontiers in oncolytic virus therapy." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-ia24.

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Seibert, Krystal N., Karim Essani, and Bruce E. Bejcek. "Abstract 2716: Development of tanapox virus for oncolytic therapy." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2716.

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Carroll, Danielle, James Harper, Travers Jon, Shannon Burke, Ruth Franks, Christel Navarro, Xing Cheng, Robert Wilkinson, and Hong Jin. "Abstract 4556: MEDI5395: An armed oncolytic Newcastle disease virus." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4556.

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"Twenty Years of Progress in Oncolytic Virus Clinical Trials." In 2022 International Conference on Biotechnology, Life Science and Medical Engineering. Clausius Scientific Press, 2022. http://dx.doi.org/10.23977/blsme.2022070.

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Muik, Alexander, Janine Kimpel, Reinhard Tober, Carles Urbiola, and Dorothee von Laer. "Abstract B37: VSV-GP: A vaccine vector and oncolytic virus." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-b37.

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Reports on the topic "Oncolytic viru"

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Zhang, Xiaoliu. A Potent Oncolytic Herpes Simplex Virus for Therapy of Advanced Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada442299.

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Zhang, Xiaoliu. A Fusogenic Oncolytic Herpes Simplex Virus for Therapy of Advanced Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada444233.

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Zhang, Xiaoliu. A Fusogenic Oncolytic Herpes Simplex Virus for Therapy of Advanced Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada426841.

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Zhang, Xiaoliu. A Potent Oncolytic Herpes Simplex Virus for the Therapy of Advanced Prostate. Fort Belvoir, VA: Defense Technical Information Center, July 2006. http://dx.doi.org/10.21236/ada459160.

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Zhang, Xiaoliu. A Potent Oncolytic Herpes Simplex Virus for the Therapy of Advanced Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada429083.

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Lee, Cleo. Prostate-Specific and Tumor-Specific Targeting of an Oncolytic HSV-1 Amplicon/Helper Virus for Prostate Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, November 2009. http://dx.doi.org/10.21236/ada525082.

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