ArticleHuman gene therapy2016
Epithelial Junction Opener Improves Oncolytic Adenovirus Therapy in Mouse Tumor Models.
Article in Human gene therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- DSG2-Directed CAR-T Cells Safely and Universally Eliminate Solid Tumors.Research square · 2026Article
- Resistance to oncolytic virotherapy: Multidimensional mechanisms and therapeutic breakthroughs (Review).International journal of molecular medicine · 2025Review
- Tutorial: design, production and testing of oncolytic viruses for cancer immunotherapy.Nature protocols · 2024Review
- Mesenchymal stem cell-released oncolytic virus: an innovative strategy for cancer treatment.Cell communication and signaling : CCS · 2023Review
- Cellular resistance to an oncolytic virus is driven by chronic activation of innate immunity.iScience · 2023Article
- Article
- Development of Adenovirus Containing Liposomes Produced by Extrusion vs. Homogenization: A Comparison for Scale-Up Purposes.Bioengineering (Basel, Switzerland) · 2022Article
- Article
- Agent-based computational modeling of glioblastoma predicts that stromal density is central to oncolytic virus efficacy.iScience · 2022Article
- Translational development of a tumor junction opening technology.Scientific reports · 2022Article
- Review
- A review on the advances and challenges of immunotherapy for head and neck cancer.Cancer cell international · 2021Review
- Toxicology and biodistribution of AdAPT-001, a replication-competent type 5 adenovirus with a trap for the immunosuppressive cytokine, TGF-beta.American journal of cancer research · 2021Article
- Oncolytic Adenovirus: Prospects for Cancer Immunotherapy.Frontiers in microbiology · 2021Review
- Desmoglein-2 as a prognostic and biomarker in ovarian cancer.Cancer biology & therapy · 2020Article
- An Oncolytic Adenovirus Vector Expressing p14 FAST Protein Induces Widespread Syncytium Formation and Reduces Tumor Growth RateMolecular therapy oncolytics · 2019Article
- Targeted Delivery to Tumors: Multidirectional Strategies to Improve Treatment Efficiency.Cancers · 2019Review
- Cell-Cell Junctions Organize Structural and Signaling Networks.Cold Spring Harbor perspectives in biology · 2018Review
- Studies on the Interaction of Tumor-Derived HD5 Alpha Defensins with Adenoviruses and Implications for Oncolytic Adenovirus Therapy.Journal of virology · 2017Article
- Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
A central resistance mechanism in solid tumors is the maintenance of epithelial junctions between malignant cells that prevent drug penetration into the tumor. Human adenoviruses (Ads) have evolved mechanisms to breach epithelial barriers. For example, during Ad serotype 3 (Ad3) infection of epithelial tumor cells, massive amounts of subviral penton-dodecahedral particles (PtDd) are produced and released from infected cells to trigger the transient opening of epithelial junctions, thus facilitating lateral virus spread. We show here that an Ad3 mutant that is disabled for PtDd production is significantly less effective in killing of epithelial human xenograft tumors than the wild-type Ad3 virus. Intratumoral spread and therapeutic effect of the Ad3 mutant was enhanced by co-administration of a small recombinant protein (JO; produced in Escherichia coli) that incorporated the minimal junction opening domains of PtDd. We then demonstrated that co-administration of JO with replication-competent Ads that do not produce PtDd (Ad5, Ad35) resulted in greater attenuation of tumor growth than virus injection alone. Furthermore, we genetically modified a conditionally replicating Ad5-based oncolytic Ad (Ad5Δ24) to express a secreted form of JO upon replication in tumor cells. The JO-expressing virus had a significantly greater antitumor effect than the unmodified AdΔ24 version. Our findings indicate that epithelial junctions limit the efficacy of oncolytic Ads and that this problem can be address by co-injection or expression of JO. JO has also the potential for improving cancer therapy with other types of oncolytic viruses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.