Relevant bibliographies by topics / Oncolytic Adenoviru

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Academic literature on the topic 'Oncolytic Adenoviru'

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

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Journal articles on the topic "Oncolytic Adenoviru"

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Ho, Chun-Te, Mei-Hsuan Wu, Ming-Jen Chen, Shih-Pei Lin, Yu-Ting Yen, and Shih-Chieh Hung. "Combination of Mesenchymal Stem Cell-Delivered Oncolytic Virus with Prodrug Activation Increases Efficacy and Safety of Colorectal Cancer Therapy." Biomedicines 9, no. 5 (May 13, 2021): 548. http://dx.doi.org/10.3390/biomedicines9050548.

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Although oncolytic viruses are currently being evaluated for cancer treatment in clinical trials, systemic administration is hindered by many factors that prevent them from reaching the tumor cells. When administered systemically, mesenchymal stem cells (MSCs) target tumors, and therefore constitute good cell carriers for oncolytic viruses. MSCs were primed with trichostatin A under hypoxia, which upregulated the expression of CXCR4, a chemokine receptor involved in tumor tropism, and coxsackievirus and adenovirus receptor that plays an important role in adenoviral infection. After priming, MSCs were loaded with conditionally replicative adenovirus that exhibits limited proliferation in cells with a functional p53 pathway and encodes Escherichia coli nitroreductase (NTR) enzymes (CRAdNTR) for targeting tumor cells. Primed MSCs increased tumor tropism and susceptibility to adenoviral infection, and successfully protected CRAdNTR from neutralization by anti-adenovirus antibodies both in vitro and in vivo, and specifically targeted p53-deficient colorectal tumors when infused intravenously. Analyses of deproteinized tissues by UPLC-MS/QTOF revealed that these MSCs converted the co-administered prodrug CB1954 into cytotoxic metabolites, such as 4-hydroxylamine and 2-amine, inducing oncolysis and tumor growth inhibition without being toxic for the host vital organs. This study shows that the combination of oncolytic viruses delivered by MSCs with the activation of prodrugs is a new cancer treatment strategy that provides a new approach for the development of oncolytic viral therapy for various cancers.
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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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Phillips, Lynette, Joy Gumin, Shoudong Li, Marc Daou, Daniel Ledbetter, Anwar Hossain, Brittany Parker Kerrigan, Candelaria Gomez-Manzano, Juan Fueyo, and Frederick Lang. "TMOD-16. A NOVEL ADENOVIRAL-PERMISSIVE, IMMUNOCOMPETENT HAMSTER GLIOMA MODEL TO EVALUATE ONCOLYTIC ADENOVIRAL THERAPY." Neuro-Oncology 22, Supplement_2 (November 2020): ii231. http://dx.doi.org/10.1093/neuonc/noaa215.967.

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Abstract Oncolytic adenoviruses, including Delta-24-RGD, target tumors by direct tumor cell oncolysis and by activation of an anti-tumor immune response. Due to the species selectivity of oncolytic adenoviruses, there is currently no single preclinical animal model of glioma that supports viral replication, tumor oncolysis, and virus-mediated immune responses. To address this gap, we took advantage of the Syrian hamster to develop the first glioma model that is both adenovirus replication-permissive and immunocompetent. Hamster glioma stem-like cells (GSCs), transformed by forced expression of hTERT, SV40 large T antigen, and h-RasV12, reproducibly form intracranial tumors in hamsters. In vitro, electron microscopy and cytopathic effect assays demonstrated that hamster GSCs supported viral replication and were susceptible to Delta-24-RGD-mediated cell death. In vivo, hamster GSCs consistently developed into highly proliferative tumors resembling high-grade gliomas. Following intratumoral delivery of Delta-24-RGD, immunohistochemistry for viral proteins demonstrated viral infectivity and replication in hamster gliomas. Flow cytometry revealed increased T cell infiltration in Delta-24-RGD-infected tumors. Delta-24-RGD treatment of tumor-bearing hamsters led to significantly increased survival compared with hamsters treated with PBS. Using this model, we evaluated the effects of corticosteroid-mediated immunosuppression on Delta-24-RGD efficacy. Dexamethasone treatment significantly decreased peripheral blood lymphocytes, decreased tumor-infiltrating lymphocytes, and suppressed the levels of serum anti-adenovirus antibodies. Dexamethasone reduced the number of long-term survivors and decreased the median survival (50 days for Delta-24-RGD + dexamethasone vs undetermined for Delta-24-RGD alone). In summary, we have developed the first adenovirus-permissive, immunocompetent hamster glioma model, addressing a critical need for a model in which to study the role of direct oncolysis in driving immune mediated viral clearance versus driving an antiglioma immune response. Understanding these mechanisms is critical to optimizing the success of oncolytic adenoviral therapy in the clinic.
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Hemminki, Akseli. "Oncolytic Immunotherapy: Where Are We Clinically?" Scientifica 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/862925.

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Following a century of preclinical and clinical work, oncolytic viruses are now proving themselves in randomized phase 3 trials. Interestingly, human data indicates that these agents have potent immunostimulatory activity, raising the possibility that the key consequence of oncolysis might be induction of antitumor immunity, especially in the context of viruses harboring immunostimulatory transgenes. While safety and efficacy of many types of oncolytic viruses, including adenovirus, herpes, reo, and vaccinia seem promising, few mechanisms of action studies have been performed with human substrates. Thus, the relative contribution of “pure” oncolysis, the immune response resulting from oncolysis, and the added benefit of adding a transgene remain poorly understood. Here, the available clinical data on oncolytic viruses is reviewed, with emphasis on immunological aspects.
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Hensen, Lobke C. M., Rob C. Hoeben, and Selas T. F. Bots. "Adenovirus Receptor Expression in Cancer and Its Multifaceted Role in Oncolytic Adenovirus Therapy." International Journal of Molecular Sciences 21, no. 18 (September 17, 2020): 6828. http://dx.doi.org/10.3390/ijms21186828.

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Oncolytic adenovirus therapy is believed to be a promising way to treat cancer patients. To be able to target tumor cells with an oncolytic adenovirus, expression of the adenovirus receptor on the tumor cell is essential. Different adenovirus types bind to different receptors on the cell, of which the expression can vary between tumor types. Pre-existing neutralizing immunity to human adenovirus species C type 5 (HAdV-C5) has hampered its therapeutic efficacy in clinical trials, hence several adenoviral vectors from different species are currently being developed as a means to evade pre-existing immunity. Therefore, knowledge on the expression of appropriate adenovirus receptors on tumor cells is important. This could aid in determining which tumor types would benefit most from treatment with a certain oncolytic adenovirus type. This review provides an overview of the known receptors for human adenoviruses and how their expression on tumor cells might be differentially regulated compared to healthy tissue, before and after standardized anticancer treatments. Mechanisms behind the up- or downregulation of adenovirus receptor expression are discussed, which could be used to find new targets for combination therapy to enhance the efficacy of oncolytic adenovirus therapy. Additionally, the utility of the adenovirus receptors in oncolytic virotherapy is examined, including their role in viral spread, which might even surpass their function as primary entry receptors. Finally, future directions are offered regarding the selection of adenovirus types to be used in oncolytic adenovirus therapy in the fight against cancer.
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Peter, Malin, and Florian Kühnel. "Oncolytic Adenovirus in Cancer Immunotherapy." Cancers 12, no. 11 (November 13, 2020): 3354. http://dx.doi.org/10.3390/cancers12113354.

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Tumor-selective replicating “oncolytic” viruses are novel and promising tools for immunotherapy of cancer. However, despite their first success in clinical trials, previous experience suggests that currently used oncolytic virus monotherapies will not be effective enough to achieve complete tumor responses and long-term cure in a broad spectrum of cancers. Nevertheless, there are reasonable arguments that suggest advanced oncolytic viruses will play an essential role as enablers of multi-stage immunotherapies including established systemic immunotherapies. Oncolytic adenoviruses (oAds) display several features to meet this therapeutic need. oAds potently lyse infected tumor cells and induce a strong immunogenic cell death associated with tumor inflammation and induction of antitumor immune responses. Furthermore, established and versatile platforms of oAds exist, which are well suited for the incorporation of heterologous genes to optimally exploit and amplify the immunostimulatory effect of viral oncolysis. A considerable spectrum of functional genes has already been integrated in oAds to optimize particular aspects of immune stimulation including antigen presentation, T cell priming, engagement of additional effector functions, and interference with immunosuppression. These advanced concepts have the potential to play a promising future role as enablers of multi-stage immunotherapies involving adoptive cell transfer and systemic immunotherapies.
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Mantwill, Klaus, Florian Gerhard Klein, Dongbiao Wang, Sruthi Vasantamadhava Hindupur, Maximilian Ehrenfeld, Per Sonne Holm, and Roman Nawroth. "Concepts in Oncolytic Adenovirus Therapy." International Journal of Molecular Sciences 22, no. 19 (September 29, 2021): 10522. http://dx.doi.org/10.3390/ijms221910522.

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Oncolytic adenovirus therapy is gaining importance as a novel treatment option for the management of various cancers. Different concepts of modification within the adenovirus vector have been identified that define the mode of action against and the interaction with the tumour. Adenoviral vectors allow for genetic manipulations that restrict tumour specificity and also the expression of specific transgenes in order to support the anti-tumour effect. Additionally, replication of the virus and reinfection of neighbouring tumour cells amplify the therapeutic effect. Another important aspect in oncolytic adenovirus therapy is the virus induced cell death which is a process that activates the immune system against the tumour. This review describes which elements in adenovirus vectors have been identified for modification not only to utilize oncolytic adenovirus vectors into conditionally replicating adenoviruses (CRAds) that allow replication specifically in tumour cells but also to confer specific characteristics to these viruses. These advances in development resulted in clinical trials that are summarized based on the conceptual design.
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Reid, Tony, Andrew Kummel, Scott Caroen, Jaimin Shah, Bryan Oronsky, and Christopher Larson. "Abstract P3-07-20: Treatment of 4T1 Breast Cancer with Liposome-Encapsulated AdAPT-001, a TGF-beta Trap Encoded Oncolytic Adenovirus Currently in a Phase 1/2 Anticancer Trial." Cancer Research 83, no. 5_Supplement (March 1, 2023): P3–07–20—P3–07–20. http://dx.doi.org/10.1158/1538-7445.sabcs22-p3-07-20.

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Abstract Adenoviral vectors have been used extensively for gene therapy. However, efficient infection of cells requires expression of the coxsackie-adenoviral receptor (CAR). Many tumor cells lack adequate expression of CAR and, hence, are not good targets for adenoviral based vectors. We have developed a unique nanoparticle (Epi-039) that can be used to efficiently introduce adenoviral vectors into tumor cells that have low or no CAR expression. We used the CAR-negative 4T1 mammary carcinoma model system, which represents a typical triple-negative breast cancer cell line (ER−, PR−, HER2−) and which is refractory to adenoviral infection to demonstrate effective transduction of an encapsulated oncolytic adenovirus. The adenovirus that was used is called AdAPT-001. This armed oncolytic virus, which is currently in a phase I/II clinical trial called BETA PRIME for the treatment of refractory cancers, expresses a TGFb receptor trap to neutralize the immunosuppressive cytokine, TGF beta. Overexpression of TGF-beta positively correlates with metastasis in breast carcinoma and thus confers a poorer prognosis. In this study, the unique Epi-039 nanoparticle carrying AdAPT-001 not only significantly enhanced the transduction efficiency of AdAPT-001 but also protected it from neutralization by natural antibodies in human whole blood. Accordingly, we demonstrate a significant increase (P value= 0.0029) in the expression of green fluorescent protein (GFP) in CAR-negative 4T1 cells infected with the encapsulated AdAPT-001 adenovirus but not the unencapsulated AdAPT-001 adenovirus. Additional in vivo studies using nanoparticle encapsulated adenoviral vectors including AdAPT-001 to treat breast cancer are underway for rapid translation to the clinic. Citation Format: Tony Reid, Andrew Kummel, Scott Caroen, Jaimin Shah, Bryan Oronsky, Christopher Larson. Treatment of 4T1 Breast Cancer with Liposome-Encapsulated AdAPT-001, a TGF-beta Trap Encoded Oncolytic Adenovirus Currently in a Phase 1/2 Anticancer Trial [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr P3-07-20.
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O'Prey, Jim, Simon Wilkinson, and Kevin M. Ryan. "Tumor Antigen LRRC15 Impedes Adenoviral Infection: Implications for Virus-Based Cancer Therapy." Journal of Virology 82, no. 12 (April 2, 2008): 5933–39. http://dx.doi.org/10.1128/jvi.02273-07.

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ABSTRACT Adenoviruses for gene or oncolytic therapy are under development. Notable among these strategies is adenoviral delivery of the tumor suppressor p53. Since all therapeutics have limitations in certain settings, we have undertaken retroviral suppressor screens to identify genes conferring resistance to adenovirus-delivered p53. These studies identified the tumor antigen LRRC15, which is frequently overexpressed in multiple tumor types, as a repressor of cell death due to adenoviral p53. LRRC15, however, does not impede p53 function per se but impedes adenoviral infection. Specifically, LRRC15 causes redistribution of the coxsackievirus-adenovirus receptor away from the cell surface. This effect is manifested in less adenoviral binding to the surfaces of LRRC15-expressing cells. This discovery, therefore, not only is important for understanding adenoviral biology but also has potentially important implications for adenovirus-based anticancer therapeutics.
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Han, Zhezhu, Yeonsoo Joo, Jihyun Lee, Suwan Ko, Rong Xu, Geun-Hyeok Oh, Soojin Choi, Jeong A. Hong, Hye Jin Choi, and Jae J. Song. "High levels of Daxx due to low cellular levels of HSP25 in murine cancer cells result in inefficient adenovirus replication." Experimental & Molecular Medicine 51, no. 10 (October 2019): 1–20. http://dx.doi.org/10.1038/s12276-019-0321-4.

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Abstract When the adenoviral protein E1B55K binds death domain-associated protein (Daxx), the proteasome-dependent degradation of Daxx is initiated, and adenoviral replication is effectively maintained. Here, we show that the cellular levels of Daxx differ between human and mouse cancer cell lines. Specifically, we observed higher cellular Daxx levels and the diminished replication of oncolytic adenovirus in mouse cancer cell lines, suggesting that cellular Daxx levels limit the replication of oncolytic adenoviruses that lack E1B55K in murine cells. Indeed, the replication of oncolytic adenoviruses that lack E1B55K was significantly increased following infection with oncolytic adenovirus expressing Daxx-specific shRNA. Cellular Daxx levels were decreased in mouse cells expressing heat shock protein 25 (HSP25; homolog of human HSP27) following heat shock or stable transfection with HSP25-bearing plasmids. Furthermore, Daxx expression in murine cell lines was primarily regulated at the transcriptional level via HSP25-mediated inhibition of the nuclear translocation of the signal transducer and activator of transcription 3 (stat3) protein, which typically upregulates Daxx transcription. Conversely, human HSP27 enhanced stat3 activity to increase Daxx transcription. Interestingly, human Daxx, but not mouse Daxx, was degraded as normal by ubiquitin-dependent lysosomal degradation; however, HSP27 downregulation induced the ubiquitin-independent proteasomal degradation of Daxx.
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Dissertations / Theses on the topic "Oncolytic Adenoviru"

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TRIPODI, LORELLA. "INTESTINAL MICROBIOTA IS A MAJOR DETERMINANT IN THE RESPONSE TO ONCOLYTIC VACCINE IN A MOUSE MODEL OF MELANOMA." Doctoral thesis, Università degli Studi di Milano, 2021. http://hdl.handle.net/2434/884815.

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Cancer immunotherapy has achieved tremendous results, however the outcome of therapies targeting immune inhibitory pathways, specifically CTLA-4 and the axis between programmed cell death protein 1 (PD-1) and its ligand 1 (PD-L1) has many genetic and environmental sources of variability. Many studies demonstrated the influence of gut microbiome on immune checkpoint inhibitors (ICIs) outcome. Besides ICIs, oncolytic vaccines (OVs) are a promising therapeutic alternative in cancer immunotherapy with possible relevant contribution to treatment of several types of tumors; OVs are, in fact, able to convert immunologically “cold” tumors into “hot” ones. OVs represent an optimum candidate to combine with ICIs, increasing their response blockade both in immunogenic and poorly immunogenic tumors. We hypothesized that manipulation of intestinal gut microbiota could also affect OVs therapeutic efficacy; at this aim, we determined whether efficacy of the oncolytic adenovirus Ad5D24-CpG (Ad-CpG) therapy could be affected by the gut microbiome in a syngeneic mouse model of melanoma. Sterilization of the gut microbiota with highdose vancomycin impaired efficacy of Ad-CpG therapy, reducing the tumor-infiltrating IFN-gamma CD8 T-cell. Cohousing mice pre-treated with vancomycin and a control group, with consequent microbiota restoration, prior to treatment with Ad-CpG, ablated the negative effect of antibiotic, confirming that Ad-CpG-reduced efficacy was mediated by the intestinal microbiota. Considering the ability of Bifidobacterium as a positive regulator of antitumor immunity in vivo, by promoting pro-inflammatory signals in innate immune cells, we evaluated tumor regression in syngeneic mouse model of melanoma treated with a combination of Ad-CpG and Bifidobacterium spp. cocktail. The group receiving the combined regimen showed the best tumor control and an enrichment of bacteria belong to Firmicutes phylum, evaluated by fecal microbiome profiling by 16S rRNA. Our data indicates that gut microbiota affects the immune responses elicited by oncolytic adenovirus Ad-CpG and Bifidobacterium supplementations maximize its activity.
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Leja, Justyna. "Oncolytic Adenovirus Therapy of Neuroendocrine Tumors." Doctoral thesis, Uppsala universitet, Institutionen för immunologi, genetik och patologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-146966.

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Neuroendocrine tumors (NETs), originally described as carcinoids, represent a rare and heterogeneous group of neoplasms associated with intensive secretion of hormones, bioactive peptides and amines. Most of the patients are diagnosed at a late stage of disease, often with liver metastases. Surgery remains the main treatment to control metastatic disease, but is not curative. Oncolytic virotherapy represents a promising approach to treat cancer and different strategies have been exploited to restrict viral replication to tumor cells. We developed an oncolytic adenovirus based on serotype 5, Ad5[CgA-E1A], where the chromogranin A (CgA) promoter controls expression of the E1A gene and thereby virus replication. We found that Ad5[CgA-E1A], selectively replicates in NET cells and it is able to suppress fast-growing human BON carcinoid tumors in nude mice. The activity of Ad5[CgA-E1A] was not completely blocked in liver cells. We further repressed virus replication in hepatocytes by targeting E1A with miR122, an miRNA specifically expressed in the liver. miRNAs bind to mRNA and induce its cleavage or translational blockage. By insertion of tandem repeats of miR122 target sequences in 3’UTR of E1A gene, we observed reduced E1A protein expression and replication arrest in miR122 expressing liver cells. The oncolytic potency of the miR122-targeted virus was not affected in NET cells. Since some NET and neuroblastoma cells express high levels of somatostatin receptors (SSTRs), we introduced in the virus fiber knob cyclic peptides, which contain four amino acids (FWKT) and mimic the binding site of somatostatin for SSTRs. The FWKT-modified Ad5 transduces midgut carcinoid cells from liver metastases about 3-4 times better than non-modified Ad5. Moreover, FWKT-modified Ad5 overcomes neutralization in an ex vivo human blood loop model to a greater extent than Ad5, indicating that the fiber knob modification may prolong the systemic circulation time. NETs represent a huge therapeutic challenge and novel diagnostic markers are needed for early detection and effective treatment of NETs. We have profiled primary tumors and liver metastases of ileocaceal NETs, using Affymetrix microarrays and advanced bioinformatics. We have identified six novel marker genes and show high similarity between primary lesions and liver metastases transcriptome by hierarchical clustering analysis.
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Alqahtani, Ali Saeed. "Investigation of a potentially novel oncolytic adenovirus." Thesis, University of Bristol, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.687423.

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In order to investigate protein V binding partners and the cellular pathways modulated by protein V, affinity purification coupled with SILAC based quantitative proteomics was used to determine the viral and cellular protein(s) binding to adenovirus protein V. This analysis indicates that the viral protein IVa2 and three cellular proteins (C1QBP, KNPA4 and PARP1) may bind to adenovirus protein V. Furthermore, quantitative proteomics and RNAseq techniques were combined to examine the response of cellular proteins and genes in A549 and WI-38 cells infected by Ad5-dVrTSB compared to wild type Ad5 and rAd5-EGFP. Interestingly, I found that PARP1 and C1QBP were moderately increased by wild type Ad5 infection in both cell lines, but remained unchanged with Ad5-dVrTSB and rAd5-EGFP infection. Furthermore, PARP1 knockdown experiments indicated that PARP1 could make a small positive contribution to wild type Ad5 replication, but not for Ad5-dVrTSB replication. Finally, C1QBP knockdown experiments showed that C1QBP may play a role in inhibiting wild type Ad5 replication.
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Thoma, Clemens Matthias Manuel. "Improving intraperitoneal adenovirus virotherapy for ovarian cancer." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:841e4334-f408-4da3-b8e6-1d29350c5304.

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The use of intraperitoneal (i.p.) adenovirus virotherapy of ovarian cancer is currently limited by insufficient efficacy and high toxicity. Both factors are associated with adenovirus serotype 5 (Ad5) in this setting and may be serotype-specific. Low levels of uptake receptors (CAR and αV integrins) on ovarian tumour cells and widespread immunity against Ad5 among patients appear to restrict efficacy and intraperitoneal inflammatory responses against Ad5 were among the reasons for the termination of a phase II/III clinical trial in ovarian cancer. This thesis sought to overcome these obstacles by investigating the alternative adenovirus serotypes Ad3 and Ad11. For these viruses lower pre-existing antiviral immunity and utilisation of different uptake receptors have been reported. Furthermore, virus cloaking with novel polymers which could impart enhanced protection from neutralisation was examined. In vitro, wild-type Ad3, Ad5 and Ad11 displayed differential oncolytic activity in a panel of ovarian cancer cell lines which partly correlated to uptake receptor expression and virus internalisation. However, some cell lines displayed lysis resistance in a serotype-specific manner. While the inflammatory response six hours after i.p. administration of Ad11 in CD46-transgenic mice did not differ from Ad5, in long-term studies of repeated administration Ad5 induced significantly more severe pathologic effects in the form of adhesions and liver toxicity than Ad11 or mock-treatment. Oncolysis inhibition assays using malignant exudate samples demonstrated greater neutralisation of Ad3 and Ad5 in comparison to Ad11 at low concentrations of samples. Notably, 10-fold less Ad11 than Ad5 was required for oncolytic efficacy at a sample concentration of 10%. In an ex vivo model of ascites from ovarian cancer patients Ad5 modified with novel polymer formulations achieved at least 50% cell kill in six of eight samples, in contrast to two of eight samples for non-modified Ad5. These data suggest that virotherapy using Ad11 might be advantageous over Ad3 or Ad5. The lack of strong inflammation and the possibility to decrease treatment doses due to less neutralisation of Ad11 might result in considerably improved patient safety. Chemical modification of Ad with novel polymers presents an exciting advancement in overcoming treatment neutralisation in adenovirus virotherapy.
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Clarkin, Ryan Gregory. "Enhancing Oncolytic Adenovirus Vector Efficacy through Co-expression of the p14 Fusion-associated Small Transmembrane Protein and Adenovirus Death Protein." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/38379.

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Conditionally-replicating adenoviruses (CRAds) have generally demonstrated only modest therapeutic efficacy in human clinical trials, in part due to their poor ability to spread throughout a tumor mass. In these studies, I first examined whether inclusion of an intact early region 3 (E3) and the p14 fusion-associated small transmembrane (FAST) protein in a CRAd vector can enhance oncolytic efficacy by improving viral spread. E3 encodes the adenovirus death protein (ADP), which enhances virus progeny release from infected cells, while p14 FAST can allow spread of the virus through cell-cell fusion. I generated viruses with (CRAdRC109) or without (CRAdRC111) an intact E3 region, which encoded the p14 FAST gene between the fiber coding sequence and E4 region of their viral genomes. In the A549 human lung cancer cell line, both CRAdRC109 and CRAdRC111 expressed p14 FAST at very low levels when compared to CRAdFAST, a similar virus that expressed the protein from within the E3 deletion, and thus had a relatively poor ability to mediate cell-cell fusion. Although inclusion of E3/ADP in CRAdRC109 did result in larger plaques and increased virus spread relative to CRAdRC111, neither virus showed improved oncolytic activity relative to CRAdFAST. I subsequently developed CRAdRC116, in which the E3 region of the viral genome was replaced with a bicistronic expression cassette containing the p14 FAST and ADP coding sequences separated by a self-cleaving 2A peptide sequence. This virus co-expressed p14 FAST and ADP and caused extensive cell-cell fusion in A549 cells. However, expression of ADP from CRAdRC116 did not increase cancer cell killing nor virus spread, and thus did not enhance oncolytic efficacy relative to CRAdFAST. These studies suggest that p14 FAST and ADP do not exhibit synergy when co-expressed from a CRAd vector. Future studies should instead focus on combining other methods of improving viral spread in conjunction with expression of ADP or FAST proteins from CRAd.
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Cooper, Lisa May. "Bioprocessing of oncolytic group B adenovirus for scalable production." Thesis, University of Oxford, 2014. https://ora.ox.ac.uk/objects/uuid:bc62bd13-f43f-4d35-8975-7fc341ce209c.

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The central aim of this thesis was to develop strategies to improve the manufacture of the group B chimeric oncolytic adenovirus, ColoAd1, which rapidly kills and lyses host cells. In attempting to improve the cellular yield of ColoAd1, this thesis therefore sought to identify host infection-related factors that limited ColoAd1 production. In the widely-used manufacturing cell line, HEK293, ColoAd1 replication depleted intracellular ATP earlier than Ad11p and activated the intracellular energy sensor, AMPK. This might have reflected earlier ATP depletion, or possibly the absence of the E4orf4 protein from ColoAd1 compared to Ad11p. Despite this difference in AMPK activation, both viruses appeared able to maintain mTORC1 activity, which may be essential particularly for protein synthesis in the early stages of virus infection. For production purposes, preventing intracellular ATP depletion was seen as an attractive mechanism of maintaining ColoAd1 infected host cell viability and was hypothesised to lead to increased virus yield. A range of strategies were explored to enhance depleting ATP levels. Even though none of these were dramatically successful, they indicated that perhaps the anabolic building blocks required for viral replication were more important than cellular energy levels. Finally, a screening methodology based on siRNA knockdown was used to identify kinases that affected ColoAd1 replication. Many hits were identified, and several candidate kinases indicated a role for intracellular calcium signalling limiting virus particle production. Overall, data presented in this thesis supports the manufacture of ColoAd1 in HEK293 cells and suggest that enhancing glycolysis may increase ColoAd1 yield. It also provides mechanistic insights into the replication of ColoAd1 and Ad11p that may inform the improved design of group B oncolytic adenoviruses.
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Silver, Jim. "Replication-competent adenovirus 11p vector as a new oncolytic agent." Doctoral thesis, Umeå universitet, Virologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-50773.

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Human adenoviruses (Ads) as vectors have been studied for cancer gene therapy for several decades due to their ability to shut down host cell replication and lyse tumour cells. Ad5 of species C is commonly used as a replication-defective or a replication-competent vector. However, many tumour cells are relatively refractory to infection by Ad5 since the cells lack the viral receptor CAR. Thus, species B Ads are becoming more important as alternative vectors since they use CD46 as primary receptor, the expression of which is up-regulated on many tumour cell surfaces, and they also have low seroprevalence in humans. Although Ad3, Ad7, Ad11 and Ad35 have been altered to become replication-defective vectors, investigations based on replicating adenovirus vectors are still warranted.   The major aim of this thesis has been to characterize the transduction efficacy and oncolytic effect of the replication-competent adenovirus 11pGFP vector (RCAd11pGFP) in human solid tumour cell lines. Evaluation of the vector would ultimately help us to understand whether the tumour cells affect virus replication and whether the vector replicates differently in tumour cells and in untransformed diploid cells, and would eventually lead to development of more potent oncolytic adenoviruses for treatment of human cancers. The Ad11-based vector RCAd11pGFP consists of the entire Ad11p genome with a green fluorescence protein (GFP) expression cassette inserted. RCAd11pGFP shows all the characteristics of the wild-type virus and expresses GFP in cells four hours p.i. Antisera raised against Ad11p virions and hexons were able to neutralize RCAd11pGFP infection but antiserum raised against the Ad11p fibre knob could not. The infection is reduced by 90% but the fibre knob antiserum cannot completely block virus infection. Initial screening of the infection capacity of five wild-type adenoviruses in four colon cancer cell lines revealed that Ad11p, Ad11a and Ad35 of species B, showed similar replication kinetics but Ad5 showed delayed onset of virus replication in comparison to species B Ads. These data support the use of Ad11p as an alternative vector for treatment of colon cancer. The transduction efficiency of RCAd11pGFP in colon cancer and prostate cancer cell lines was studied using flow cytometry assay (FACS), and this showed that the cytolytic effect was not always in accordance with GFP expression. Toxicity assay and virus one-step replication assay showed that RCAd11pGFP replicates in highly tumorigenic cell lines (HT29, T84 and PC-3) to a greater extent than less tumorigenic cell lines (LS174T, HCT-8, DU145 and LNCaP cells), even though the latter showed relatively high GFP expression. This initial finding led to the subsequent discovery of CEACAM-family molecules, which were highly expressed in HT29 and T84 cells. Interestingly, the Ad5 wild-type virus did not manifest the same tumour-specific replication that RCAd11pGFP did in the cell lines studied. Furthermore, we investigated the influence of tumour markers for RCAd11pGFP replication in colon cancer cells. A double-staining FACS assay for detecting members of CEACAM-family molecules was established and we found that the levels of CEACAM6 were up-regulated in the cells infected by RCAd11pGFP or Ad11pwt relative to uninfected cells. However, this virus replication could not be suppressed by CEACEA6 siRNA. Our results indicate that several tumour markers or factors might be involved in promoting propagation of the virus. In vivo experiments showed significant growth inhibition of T84 and HT-29 tumours in xenograft mice treated with either RCAd11pGFP or Ad11pwt, compared to untreated controls. Furthermore, the role of the anti-tumour effect of RCAd11pGFP was also confirmed in PC3 prostate tumours in BALB/c mice. In conclusion, the novel RCAd11pGFP vector was shown to have an anti-tumour effect in vitro and in vivo. This tumour-killing effect could be enhanced in highly tumorogenic cells through virus replication. Consequently, RCAd11p may lead to development of a more potent and useful vector for human cancer therapy.
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Del, Papa Joshua. "Assessing the Oncolytic Capacity of Conditionally Replicating Adenovirus Armed with p14 Fusion Associated Small Transmembrane Protein and the Adenovirus Death Protein." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39485.

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Intratumoral injection of oncolytic viruses provides a direct means of tumor cell elimination for inoperable tumors. Unfortunately, oncolytic vectors based on human adenovirus (HAdV) typically do not spread efficiently throughout the tumor mass, reducing the efficacy of treatment. In this thesis, I explore the efficacy of conditionally replicating HAdV vectors expressing either the p14 Fusion Associated Small Transmembrane (FAST) protein (CRAdFAST) or p14 FAST protein in combination with the adenovirus death protein (CRAdFAST-ADP). The p14 FAST protein mediates cell-cell fusion, which may enhance spread of the virus-mediated, tumor cell-killing effect, while ADP aids in cell lysis and HAdV spread at late times in infection. I first explored the efficacy of CRAdFAST in the 4T1 immune competent mouse model of cancer. Treatment with CRAdFAST resulted in enhanced cell death compared to vector lacking the p14 FAST gene in vitro, but did not reduce the tumor growth rate in vivo. The 4T1 model was significantly resistant to HAdV infection and propagation, so I next explored CRAdFAST efficacy in human A549 cell culture and a xenograft mouse model of cancer. In the human A549 lung adenocarcinoma model of cancer, CRAdFAST showed significantly improved oncolytic efficacy in vitro and in vivo. In an A549 xenograft tumor model in vivo, CRAdFAST induced tumor cell fusion which led to the formation of large acellular regions within the tumor, and significantly reduced the tumor growth rate compared to control vector. Finally, to assess the use of a newly constructed CRAdFAST vector co-expressing the adenovirus death protein (ADP), a new model was explored comprised of CMT-64.6 mouse lung carcinoma cells which are syngeneic with Balb/C mice. This model was significantly more sensitive to HAdV infection and CRAdFAST induced fusion than the 4T1 cell line. In this model, expression of ADP and p14 FAST from a CRAdFAST-like vector (CRAdFAST-ADP) resulted in significant oncolytic synergy in vitro but not in vivo. My results indicate that expression of p14 FAST protein, and potentially ADP, from an oncolytic HAdV can improve vector efficacy for the treatment of cancer, but improved in vivo models will be required to analyze the full preclinical potential of these oncolytic HAdV vectors.
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Herod, Morgan Reece. "Oncolytic adenovirus vectors for nitroreductase suicide gene therapy of prostate cancer." Thesis, University of Birmingham, 2010. http://etheses.bham.ac.uk//id/eprint/957/.

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Prostate cancer is the most common male cancer in the UK and USA, with a 1/13 chance of diagnosis and a 1/30 lifetime risk of death from the disease. Current treatment options include radiotherapy, surgery and hormone therapy, however 1/3 patients escape from all therapies and novel therapies are urgently required for this patient group. The University of Birmingham gene therapy group constructed two oncolytic adenovirus vectors, CRAd-NTR and vNR6, both of which contained the E1B-55K deletion and expressed the transgene nitroreductase for combined oncolytic virotherapy and enzyme/prodrug gene therapy. The latter of these two vectors, vNR6, expressing nitroreductase from the pIX virus promoter demonstrated the greatest cytotoxicity at low virus concentrations however also showed some lytic activity to non-transformed human fibroblasts. Our collaborators at the Institut Català d'Oncologia designed a panel of oncolytic adenovirus vectors with the E1A CR2 24 deletion and the E1A promoter replaced by an insulated E2F-1 promoter. The latest two in this series of vectors, termed ICOVIR-5 and ICOVIR-7, provide potential oncolytic backbones for the introduction of the therapeutic transgene nitroreductase. The aim of this thesis was therefore to ‘arm’ the ICOVIR based vectors with nitroreductase for combined oncolytic virotherapy and enzyme/prodrug therapy. At the beginning of this study no reports were published with either ICOVIR-5 or ICOVIR-7 based vectors. It was therefore first decided to construct both vectors expressing the marker transgene eGFP. These vectors were characterised in terms of cytotoxicity, transgene expression, DNA replication and E1A expression. Furthermore, these vectors were compared to the vNR3, an E1B-55K deleted virus similar to vNR6, but the eGFP ORF replacing that of pIX. The ICOVIR-7 based vectors were identified as being the most tumour selective vectors and demonstrated no cytotoxicity to non-transformed human fibroblasts, and were therefore chosen for the introduction of the therapeutic transgenes. The new ICOVIR-7 based vectors were constructed to express either wildtype, double mutant or triple mutant nitroreductase. Double and triple mutant nitroreductase are two previously characterised mutant nitroreductases, which show enhanced catalytic activity for the prodrug CB1954. The new nitroreductase expressing ICOVIR-7 vectors were characterised in terms of virus mediated cytotoxicity, tumour selectivity, E1A and NTR expression and cytotoxicity with the prodrug CB1954. One vector, expressing double mutant nitroreductase, showed the highest tumour selectivity and greatest combined cytotoxicity with the prodrug CB1954. Furthermore, this vector showed greater tumour selectivity and combined cytotoxicity than the E1B-55K deleted vector vNR6.
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Weigert, Melanie. "Investigating the role of programmed necrosis in oncolytic adenovirus-induced death." Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8054/.

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Oncolytic viruses are a group of viruses that preferentially replicate in cancer cells and are a promising cancer treatment. However, how these oncolytic adenoviruses kill cancer cells is not fully understood. It was long thought that DNA viruses utilize apoptosis to induce cell death but there is now evidence that adenovirus and vaccinia cytotoxicity displays features of necrosis-like programmed cell death. In order to investigate the role of necrosis in cell death as a result of oncolytic adenovirus infection, a panel of ovarian cancer cells with varying sensitivities to the oncolytic adenoviral mutant dl922-947 was used. Cells infected with dl922- 947 displayed key features of necrotic death. Using necrosis inhibitors necrostatin-1, necrosulfonamide, GSK2791840B, GSK2399872B and GSK2393843A, as well as RNAi-mediated knockdown of RIPK1, RIPK3 or MLKL, I showed that cells undergo RIPK3-dependent necrosis and that blockage of the downstream effector mixed lineage kinase domain-like (MLKL) attenuated cell death. While Tumour necrosis factor-α (TNF-α)-induced programmed necrosis(Laster, Wood and Gooding 1988) relies on the (RHIM)-dependent interaction of RIPK1 and RIPK3 (Li et al. 2012, Wu et al. 2014), RIPK1 seems to be redundant for adenovirus-induced death. Further, the addition of TNF-α blocking antibody to virus-infected cells showed no effect on either cell death. Using a RIPK3 overexpression model, I showed that the amount adenovirus- induced cell death correlated with the amount of RIPK3 expression and that RIPK3 expression did not affect virus production, infectivity or the expression of viral proteins. Further, in vivo experiments using human xenografts showed that expression of RIPK3 significantly improved anti-tumour activity following intra-tumoural injection of dl922-947.
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Books on the topic "Oncolytic Adenoviru"

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Oncolytic viruses: Methods and protocols. New York: Humana Press, 2012.

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Kirn, David H., Stephen H. Thorne, and Ta-Chiang Liu. Oncolytic Viruses: Methods and Protocols. Humana Press, 2016.

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Book chapters on the topic "Oncolytic Adenoviru"

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Tagawa, Masatoshi. "Oncolytic Adenovirus." In Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_4227-5.

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Tagawa, Masatoshi. "Oncolytic Adenovirus." In Encyclopedia of Cancer, 3218–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_4227.

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Tagawa, Masatoshi. "Oncolytic Adenovirus." In Encyclopedia of Cancer, 2623–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4227.

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Gil-Hoyos, Raul, Juan Miguel-Camacho, and Ramon Alemany. "Oncolytic Adenovirus Characterization: Activity and Immune Responses." In Adenovirus, 117–32. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-679-5_9.

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Kranzler, Justin, Matthew A. Tyler, Ilya V. Ulasov, and Maciej S. Lesniak. "Intracranial Glioma: Delivery of an Oncolytic Adenovirus." In Tumors of the Central Nervous System, Volume 1, 365–70. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0344-5_38.

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Fujiwara, Toshiyoshi. "Targeted Oncolytic Adenovirus for Human Cancer Therapy: Gene-Based Therapies for Cancer." In Gene-Based Therapies for Cancer, 79–93. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-6102-0_6.

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Ahmed, Atique U., Ilya V. Ulasov, Ronald W. Mercer, and Maciej S. Lesniak. "Maintaining and Loading Neural Stem Cells for Delivery of Oncolytic Adenovirus to Brain Tumors." In Methods in Molecular Biology, 97–109. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-340-0_8.

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Yngve, Erik, Menghan Gao, and Di Yu. "A qPCR-Based Method for Quantification of Replication Competent Adenovirus (RCA) in Conditionally Replicating Oncolytic Adenoviruses." In Methods in Molecular Biology, 249–58. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2441-8_13.

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Opyrchal, Mateusz, Ileana Aderca, and Evanthia Galanis. "Phase I Clinical Trial of Locoregional Administration of the Oncolytic Adenovirus ONYX-015 in Combination with Mitomycin-C, Doxorubicin, and Cisplatin Chemotherapy in Patients with Advanced Sarcomas." In Gene Therapy of Cancer, 705–17. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-561-9_35.

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Alemany, Ramon. "Molecular Design of Oncolytic Adenoviruses." In Adenoviral Vectors for Gene Therapy, 319–34. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-800276-6.00012-7.

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Conference papers on the topic "Oncolytic Adenoviru"

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Wechman, Stephen L., Xiao-Mei Rao, Kelly Marc McMasters, and Heshan Sam Zhou. "Abstract 3753: Improved oncolytic virotherapy by increasing adenovirus spread." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3753.

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Demiya, Koji, Hiroshi Tazawa, Yusuke Mochizuki, Miho Kure, Joe Hasei, Toshiyuki Kunisada, Yasuo Urata, Toshifumi Ozaki, and Toshiyoshi Fujiwara. "Abstract 3231: Oncolytic immunotherapy with PD-1 blockade and telomerase-specific oncolytic adenovirus in osteosarcoma." 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.am2019-3231.

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Demiya, Koji, Hiroshi Tazawa, Yusuke Mochizuki, Miho Kure, Joe Hasei, Toshiyuki Kunisada, Yasuo Urata, Toshifumi Ozaki, and Toshiyoshi Fujiwara. "Abstract 3231: Oncolytic immunotherapy with PD-1 blockade and telomerase-specific oncolytic adenovirus in osteosarcoma." 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.sabcs18-3231.

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Aoyama, Katsuyuki, Shinji Kuroda, Hiroshi Tazawa, Shunsuke Kagawa, and Toshiyoshi Fujiwara. "Abstract 719: Development of systemically-deliverable telomerase-specific oncolytic adenovirus." 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.am2014-719.

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Koodie, Lisa, Eriko Iguchi Kawakami, Kari Jacobsen, Zuzan Cayci, Andrew Taylor, Edward W. Greeno, Robert J. Schumacher, John C. Morris, Martin E. Fernandez-Zapico, and Julia Davydova. "Abstract 5925: A novel oncolytic adenovirus for radioiodine therapy and imaging." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5925.

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Miura, Yoshiaki, Julia Davydova, and Masato Yamamoto. "Abstract 5655: Infectivity selective oncolytic adenovirus for pancreatic cancer by redesigning the AB-loop via adenovirus library screening." 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.am2012-5655.

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Miura, Yoshiaki, Mizuho Sato, Julia Davydova, and Masato Yamamoto. "Abstract 724: Systemic injection of fiber-redesigned oncolytic adenovirus eliminates tumorsin vivo." 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.am2014-724.

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Sato, Mizuho, Yoshiaki Miura, and Masato Yamamoto. "Abstract 3541: Therapeutic effect of CD133-targeted oncolytic adenovirus in colon cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3541.

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Kakiuchi, Yoshihiko. "Abstract 3714: Stealth liposomes encapsulating plasmid DNA of telomerase specific oncolytic adenovirus." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3714.

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Schaumburg, Jessica C. "Abstract 4774: Engineering an oncolytic adenovirus to target CEA in colorectal cancer." 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.sabcs18-4774.

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