ArticleCancer gene therapy2009
Deletion of the E3-6.7K/gp19K region reduces the persistence of wild-type adenovirus in a permissive tumor model in Syrian hamsters.
Article in Cancer gene therapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 34 citations in OpenAlex.
- Potency-enhancing mutations in E3-19K and i-leader increase the cytolytic activity of the PH20/Molecular therapy. Oncology · 2026Article
- Comparison of the L3-23K and L5-Fiber Regions for Arming the Oncolytic Adenovirus Ad5-Delta-24-RGD with Reporter and Therapeutic Transgenes.International journal of molecular sciences · 2025Article
- Nonclinical characterization of ICVB-1042 as a selective oncolytic adenovirus for solid tumor treatment.Communications biology · 2024Article
- Neutrophils in oncolytic virus immunotherapy.Frontiers in immunology · 2024Review
- Development of Oncolytic Vectors Based on Human Adenovirus Type 6 for Cancer Treatment.Viruses · 2023Article
- Syrian hamster as an ideal animal model for evaluation of cancer immunotherapy.Frontiers in immunology · 2023Review
- A bivalent live-attenuated vaccine candidate elicits protective immunity against human adenovirus types 4 and 7.Emerging microbes & infections · 2021Article
- Review
- Arming Oncolytic Adenoviruses: Effect of Insertion Site and Splice Acceptor on Transgene Expression and Viral Fitness.International journal of molecular sciences · 2020Article
- The UPR sensor IRE1α and the adenovirus E3-19K glycoprotein sustain persistent and lytic infections.Nature communications · 2020Article
- Effect of Transgene Location, Transcriptional Control Elements and Transgene Features in Armed Oncolytic Adenoviruses.Cancers · 2020Review
- Efficacy of a new oncolytic adenovirus armed with IL-13 against oral carcinoma models.OncoTargets and therapy · 2019Article
- Pathology in Permissive Syrian Hamsters after Infection with Species C Human Adenovirus (HAdV-C) Is the Result of Virus Replication: HAdV-C6 Replicates More and Causes More Pathology than HAdV-C5.Journal of virology · 2017Article
- Oncolytic Viruses-Interaction of Virus and Tumor Cells in the Battle to Eliminate Cancer.Frontiers in oncology · 2017Review
- Safety and antitumor effect of oncolytic and helper-dependent adenoviruses expressing interleukin-12 variants in a hamster pancreatic cancer model.Gene therapy · 2015Article
- Novel permissive murine immunocompetent orthotopic colon carcinoma model for comparison of the antitumoral and safety profiles of three Adv-TKs.Gene therapy · 2014Article
- The combination of i-leader truncation and gemcitabine improves oncolytic adenovirus efficacy in an immunocompetent model.Cancer gene therapy · 2014Article
- Evaluation of monocytes as carriers for armed oncolytic adenoviruses in murine and Syrian hamster models of cancer.Human gene therapy · 2012Article
- A novel conditionally replicating adenoviral vector with dual expression of IL-24 and arresten inserted in E1 and the region between E4 and fiber for improved melanoma therapy.Cancer gene therapy · 2012Article
- Adenovirus i-leader truncation bioselected against cancer-associated fibroblasts to overcome tumor stromal barriers.Molecular therapy : the journal of the American Society of Gene Therapy · 2012Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A partial deletion of the adenovirus E3 region, comprising the overlapping 6.7K/gp19K genes, has been described for the incorporation of therapeutic genes in 'armed' oncolytic adenoviruses. This deletion allows the insertion of up to 2.5 kb genetic material into the virus and ensures strong expression of transgenes without reducing the replication and cytolytic potency of viruses in vitro. E3-gp19K and 6.7K proteins are involved in avoiding recognition and elimination of infected cells by the host immune system. Therefore, we have studied the effect of this deletion on the replication and transgene expression of the virus in immunocompetent models based on Syrian hamsters. Tumors were established by intrahepatic injection of pancreatic cancer cells with moderate (HaP-T1, HP-1) or low (H2T) permissivity for adenovirus replication. The wild-type human adenovirus 5 (Ad5) or a modified version containing the luciferase gene in the E3-6.7K/gp19K locus (Ad-WTLuc) were injected intratumorally. We found that elimination of Ad-WTLuc was faster than Ad5 in HaP-T1 and HP-1 tumors. In contrast, no differences were observed when the same tumor was established in severely immunocompromised NOD-scid IL2Rgamma(null) mice. In addition, virus-mediated luciferase expression was more stable in these animals. These results suggest that the lack of E3-6.7K/gp19K genes may accelerate the clearance of oncolytic adenoviruses in some immunocompetent tumor models.
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