ArticleJournal of virology2020
Experimental Evolution Generates Novel Oncolytic Vesicular Stomatitis Viruses with Improved Replication in Virus-Resistant Pancreatic Cancer Cells.
Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Dual role of rVSV vectors in prophylactic and therapeutic innovation: a comprehensive bibliometric and clinical trial perspective.Frontiers in immunology · 2026Pooled it
- Delivery Strategies for Oncolytic Viruses in Gastrointestinal Cancers: Progress, Mechanisms and Clinical Translations.Reviews in medical virology · 2026Review
- Bridging mechanism and clinic: unlocking the full potential of oncolytic virus-based immunotherapy.Molecular cancer · 2026Review
- Oncolytic viruses: advanced strategies in cancer therapy.Signal transduction and targeted therapy · 2026Review
- Engineering strategies to address immune and delivery barriers in pancreatic ductal adenocarcinoma: a barrier-matched translational framework.Frontiers in immunology · 2026Review
- Tumor-directed evolution of VSVΔ51M produces novel viruses with enhanced antitumor efficacy.Frontiers in molecular biosciences · 2026Article
- Directed evolution generates an oncolytic Sindbis virus with enhanced tumor-killing capacity in osteosarcoma.Molecular therapy. Oncology · 2025Article
- Vesicular Stomatitis Virus-Based Oncolytic Virotherapy: Recent Progress and Emerging Trends.Current oncology (Toronto, Ont.) · 2025Review
- Review
- Article
- Matrix Protein of Vesicular Stomatitis Virus Targets the Mitochondria, Reprograms Glucose Metabolism, and Sensitizes to 2-Deoxyglucose in Glioblastoma.Human gene therapy · 2024Article
- Fast Track Adaptation of Oncolytic Coxsackie B3 Virus to Resistant Colorectal Cancer Cells - a Method to Personalize Virotherapy.Biological procedures online · 2024Article
- Sendai virus is robust and consistent in delivering genes into human pancreatic cancer cells.Heliyon · 2024Article
- Safety and dose escalation of the targeted oncolytic adenovirus OBP-301 for refractory advanced liver cancer: Phase I clinical trial.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Vesicular Stomatitis Virus (VSV) G Glycoprotein Can Be Modified to Create a Her2/Neu-Targeted VSV That Eliminates Large Implanted Mammary Tumors.Journal of virology · 2023Article
- Directed natural evolution generates a next-generation oncolytic virus with a high potency and safety profile.Nature communications · 2023Article
- Directed Evolution of Seneca Valley Virus in Tumorsphere and Monolayer Cell Cultures of a Small-Cell Lung Cancer Model.Cancers · 2023Article
- Cellular resistance to an oncolytic virus is driven by chronic activation of innate immunity.iScience · 2023Article
- RIG-I-mediated innate immune signaling in tumors reduces the therapeutic effect of oncolytic vesicular stomatitis virus.Thoracic cancer · 2023Article
- The G285S mutation in nsP1 is sufficient to render Sindbis virus as a stable vector for gene delivery.Frontiers in microbiology · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Vesicular stomatitis virus (VSV) based oncolytic viruses are promising agents against various cancers. We have shown that pancreatic ductal adenocarcinoma (PDAC) cell lines exhibit great diversity in susceptibility and permissibility to VSV. Here, using a directed evolution approach with our two previously described oncolytic VSV recombinants, VSV-p53wt and VSV-p53-CC, we generated novel oncolytic VSVs with an improved ability to replicate in virus-resistant PDAC cell lines. VSV-p53wt and VSV-p53-CC encode a VSV matrix protein (M) with a ΔM51 mutation (M-ΔM51) and one of two versions of a functional human tumor suppressor, p53, fused to a far-red fluorescent protein, eqFP650. Each virus was serially passaged 32 times (which accounts for more than 60 viral replication cycles) on either the SUIT-2 (moderately resistant to VSV) or MIA PaCa-2 (highly permissive to VSV) human PDAC cell lines. While no phenotypic changes were observed for MIA PaCa-2-passaged viruses, both SUIT-2-passaged VSV-p53wt and VSV-p53-CC showed improved replication in SUIT-2 and AsPC-1, another human PDAC cell line also moderately resistant to VSV, while remaining highly attenuated in nonmalignant cells. Surprisingly, two identical VSV glycoprotein (VSV-G) mutations, K174E and E238K, were identified in both SUIT-2-passaged viruses. Additional experiments indicated that the acquired G mutations improved VSV replication, at least in part due to improved virus attachment to SUIT-2 cells. Importantly, no mutations were found in the M-ΔM51 protein, and no deletions or mutations were found in the p53 or eqFP650 portions of virus-carried transgenes in any of the passaged viruses, demonstrating long-term genomic stability of complex VSV recombinants carrying large transgenes.
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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.