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Dalton, Tanner; Doubrovina, Ekaterina; Pankov, Dmitry; Reynolds, Raymond; Scholze, Hanna; Selvakumar, Annamalai; Vizconde, Teresa; Savalia, Bhumesh; Dyomin, Vadim; Weigel, Christoph; Oakes, Christopher C.; Alonso, Alicia; Elemento, Olivier; Pan, Heng; Phillip, Jude M.; O'Reilly, Richard J.; Gewurz, Benjamin E.; Cesarman, Ethel; Giulino-Roth, Lisa
Blood, 05/2020, Volume: 135, Issue: 21Journal Article
Despite advances in T-cell immunotherapy against Epstein-Barr virus (EBV)-infected lymphomas that express the full EBV latency III program, a critical barrier has been that most EBV+ lymphomas express the latency I program, in which the single Epstein-Barr nuclear antigen (EBNA1) is produced. EBNA1 is poorly immunogenic, enabling tumors to evade immune responses. Using a high-throughput screen, we identified decitabine as a potent inducer of immunogenic EBV antigens, including LMP1, EBNA2, and EBNA3C. Induction occurs at low doses and persists after removal of decitabine. Decitabine treatment of latency I EBV+ Burkitt lymphoma (BL) sensitized cells to lysis by EBV-specific cytotoxic T cells (EBV-CTLs). In latency I BL xenografts, decitabine followed by EBV-CTLs results in T-cell homing to tumors and inhibition of tumor growth. Collectively, these results identify key epigenetic factors required for latency restriction and highlight a novel therapeutic approach to sensitize EBV+ lymphomas to immunotherapy. •A high-throughput screen identified hypomethylating agents as inducers of latency III viral antigens in latency I EBV+ BL.•Induction of latency III antigens in BL sensitizes resistant tumors to T-cell–mediated lysis with EBV-specific cytotoxic T lymphocytes. Display omitted
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