{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T03:17:53Z","timestamp":1790306273486,"version":"4.1.0"},"reference-count":51,"publisher":"American Society of Hematology","issue":"24","license":[{"start":{"date-parts":[[2025,2,26]],"date-time":"2025-02-26T00:00:00Z","timestamp":1740528000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,6,12]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>Despite the approval of several new treatments for patients with B-cell lymphoma, there is still a large unmet need. Diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL) are the 2 most common B-cell lymphoma subtypes, accounting for \u223c50% of all cases. EZH2 heterozygous gain-of-function somatic driver mutations are frequently found in germinal center B-cell DLBCLs and FLs. An EZH2 inhibitor has shown durable responses in patients with relapsed or refractory FL, however a considerable fraction of the patients did not show an objective response. To identify alternative therapeutic strategies, we performed CRISPR\/Cas9 knockout screens in B-cell lymphoma cells treated with or without an EZH2 inhibitor. This led to the identification of the histone methyltransferase DOT1L as a potential therapeutic target. Specifically, we showed that an EZH2 inhibitor synergizes with a DOT1L inhibitor in a panel of B-cell lymphoma cell lines regardless of the EZH2 mutation status. Mechanistically, we demonstrated that the 2 inhibitors cooperatively suppress DOT1L-regulated cell cycle genes, upregulate genes involved in interferon signaling, including antigen presenting genes, and ultimately drive B-cell differentiation by derepressing EZH2-regulated plasma cell signature genes. Furthermore, we demonstrated the effectiveness of this epigenetic combination strategy in a xenograft model, which led to significant abrogation of tumor growth. Together, our studies provide preclinical proof-of-concept for an epigenetic combination therapy to overcome resistance and improve durability of response for the treatment of B-cell lymphoma, warranting clinical investigation and illustrating an important convergent role of EZH2 and DOT1L in B-cell lymphomagenesis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1182\/blood.2024026534","type":"journal-article","created":{"date-parts":[[2025,2,26]],"date-time":"2025-02-26T12:12:08Z","timestamp":1740571928000},"page":"2873-2886","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":19,"title":["Synergistic antitumor effect of combined EZH2 and DOT1L inhibition in B-cell lymphoma"],"prefix":"10.1182","volume":"145","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5898-0043","authenticated-orcid":false,"given":"Van Thuy Mai","family":"Nguyen","sequence":"first","affiliation":[{"name":"1Division of Cell and Molecular Biology, The 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