Review uncovers shared oncogenic pathways and immune evasion in Epstein-Barr virus-related cancers, implying new therapeutic strategies.
Epstein-Barr virus (EBV) is associated with a wide spectrum of lymphoid and epithelial malignancies. This review provides a comprehensive pan-tumor perspective on the convergent oncogenic mechanisms, immune microenvironment characteristics, and shared therapeutic vulnerabilities across EBV-related cancers. We systematically summarize EBV infection and latency patterns, highlighting key shared signaling networks (e.g., NF-κB, PI3K/AKT) alongside nuanced immune evasion strategies, such as HLA modulation and steric immune blockade. By bridging these molecular insights with clinical translation, we evaluate emerging therapeutic paradigms, including immune checkpoint inhibitors, EBV-specific T-cell therapies, neutralizing antibodies, and mRNA vaccines. Ultimately, this synthesis underscores the potential of exploiting shared viral vulnerabilities to develop pan-tumor targeted therapies, offering a strategic roadmap for future clinical development.
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Wang et al. (2026) studied this question.
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