ArticleCancer immunology, immunotherapy : CII2025
BAP1 as a predictive biomarker of therapeutic response to oncolytic vaccinia virus for metastatic renal cell carcinoma therapy.
Article in Cancer immunology, immunotherapy : CII, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Recent advances in oncolytic virotherapy: insights from clinical trials and combination treatment strategies.Virology journal · 2026Review
- The α-Gal Epitope (Galα1-3Galβ1-4GlcNAc) as Therapeutic Agent in Cancer Immunotherapy, Vaccine Effectiveness Amplification and Injured Tissue Regeneration.International journal of molecular sciences · 2026Review
- The emerging role of oncolytic virotherapy in genitourinary malignancies.Frontiers in cell and developmental biology · 2026Review
- The fall of the genome protectors triad: PBRM1, SETD2, and BAP1's impact on metabolism and immunity in clear cell renal cell carcinoma.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
7 authors.
Funding
Abstract
backgroundThe therapeutic efficacy of oncolytic vaccinia virus (JX-594) has been demonstrated in metastatic clear cell renal cell carcinoma (ccRCC); however, only selected patients respond, and there are no predictive biomarkers for therapeutic response. We aimed to identify predictive biomarkers for JX-594 treatment and elucidate the underlying mechanisms.
methodsFour cell line-derived xenograft (CDX) models were developed using representative ccRCC cell lines harboring common mutations. Tumors were subcutaneously implanted into the right flank of BALB/c nude mice. Mice were treated with vehicle or JX-594 via intratumoral injection on days 0, 3, and 6, and tumor growth was evaluated. Therapeutic efficacies of JX-594 and a STING agonist were compared in the BAP1-mutant (769-P) CDX model.
resultsAll four CDX models showed significant tumor shrinkage following JX-594 treatment versus control. JX-594 exhibited greater efficacy than the STING agonist in BAP1-deficient xenografts. The BAP1 mutation was associated with rapid tumor progression and a stronger response to JX-594. JX-594 induced IFN-β expression through IRF7-dependent signaling in BAP1-deficient cells, bypassing impaired STING-IRF3 signaling.
conclusionsWe identified BAP1 as a potential predictive biomarker for JX-594 treatment and explored its underlying mechanisms. However, given that the study used immunodeficient models, the findings reflect tumor-intrinsic interferon responses and require further validation in immunocompetent models to assess immune microenvironment modulation and clinical relevance.
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