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Differential Susceptibility of Ex Vivo Primary Glioblastoma Tumors to Oncolytic Effect of Modified Zika Virus. | LitMetric

AI Article Synopsis

  • Glioblastoma (GBM) is a highly aggressive brain cancer with limited treatment options, necessitating research into new therapies.
  • An attenuated strain of the Zika virus (ZOL-1) has been developed, showing safety in mouse models and ability to target GBM stem cells effectively.
  • The study reveals that ZOL-1 can kill GBM cells in susceptible tumors and, when combined with PI3K-AKT inhibitors, enhances treatment efficacy in non-susceptible tumors, positioning ZOL-1 as a promising therapy for GBM patients.

Article Abstract

Glioblastoma (GBM), the most common primary malignant brain tumor, is a highly lethal form of cancer with a very limited set of treatment options. High heterogeneity in the tumor cell population and the invasive nature of these cells decrease the likely efficacy of traditional cancer treatments, thus requiring research into novel treatment options. The use of oncolytic viruses as potential therapeutics has been researched for some time. Zika virus (ZIKV) has demonstrated oncotropism and oncolytic effects on GBM stem cells (GSCs). To address the need for safe and effective GBM treatments, we designed an attenuated ZIKV strain (ZOL-1) that does not cause paralytic or neurological diseases in mouse models compared with unmodified ZIKV. Importantly, we found that patient-derived GBM tumors exhibited susceptibility (responders) and non-susceptibility (non-responders) to ZOL-1-mediated tumor cell killing, as evidenced by differential apoptotic cell death and cell viability upon ZOL-1 treatment. The oncolytic effect observed in responder cells was seen both in vitro in neurosphere models and in vivo upon xenograft. Finally, we observed that the use of ZOL-1 as combination therapy with multiple PI3K-AKT inhibitors in non-responder GBM resulted in enhanced chemotherapeutic efficacy. Altogether, this study establishes ZOL-1 as a safe and effective treatment against GBM and provides a foundation to conduct further studies evaluating its potential as an effective adjuvant with other chemotherapies and kinase inhibitors.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10572118PMC
http://dx.doi.org/10.3390/cells12192384DOI Listing

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