Oncolytic virotherapy and chemotherapeutic approaches against fibrosarcoma 2928
Abstract Description Fibrosarcoma is a type of rare and poorly studied cancer associated with a ∼40% survival rate at five years after diagnosis. Oncolytic virotherapy, which relies on the use of viruses to kill cancer cells, is being explored as a therapeutic agent against common cancers that show resistance to chemotherapy. One oncolytic virus, Reovirus, has been shown in clinical trials to effectively kill various types of cancer cells while having minimal side effects in patients. However, the oncolytic potential of Reovirus against rare cancers remains largely understudied. Here, we explored the oncolytic potential of genetically-different Reovirus strains in human HT-1080 fibrosarcoma cells. Our research shows that HT-1080 cells are permissive to Reovirus infection and that the infection rate is strain-specific. We quantified the ability of the different viral strains to kill fibrosarcoma cells and assessed their therapeutic effects of combining Reovirus with chemotherapeutics. Our data demonstrates that infection of HT-1080 cells with selected Reovirus strains followed by treatment with chemotherapy results in a significant decrease in cell viability compared to individual treatments. Altogether, we identified two viral strains with strong oncolytic potential in fibrosarcoma cells and demonstrated their enhanced effectiveness when used in combination with common chemotherapeutic agents. Funding Sources Supported by Elon University and NCICU (North Carolina Independent Colleges and Universities) Topic Categories Tumor Immunology: Checkpoints, Prevention, and Treatment (TIPT)
Authors
- Efraín E. Rivera-Serrano (ORCID: https://orcid.org/0000-0002-1039-7182)
- Charlotte Dagli
Institutions
- Elon University (US)
Publication Details
- Journal
- The Journal of Immunology
- Published
- 2025-11-01
- DOI
- https://doi.org/10.1093/jimmun/vkaf283.785
- Primary Topic
- Virus-based gene therapy research
- Type
- article
- Field-Weighted Citation Impact
- 0.00