{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T19:36:52Z","timestamp":1788377812051,"version":"build-2803163510"},"reference-count":36,"publisher":"American Society of Hematology","issue":"23","license":[{"start":{"date-parts":[[2022,8,12]],"date-time":"2022-08-12T00:00:00Z","timestamp":1660262400000},"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":[[2022,12,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Peripheral T-cell lymphoma (PTCL) is a heterogeneous group of hematological cancers arising from the malignant transformation of mature T cells. In a cohort of 28 PTCL cases, we identified recurrent overexpression of MYCN, a member of the MYC family of oncogenic transcription factors. Approximately half of all PTCL cases was characterized by a MYC expression signature. Inducible expression of MYCN in lymphoid cells in a mouse model caused T-cell lymphoma that recapitulated human PTCL with an MYC expression signature. Integration of mouse and human expression data identified EZH2 as a key downstream target of MYCN. Remarkably, EZH2 was found to be an essential cofactor for the transcriptional activation of the MYCN-driven gene expression program, which was independent of methyltransferase activity but dependent on phosphorylation by CDK1. MYCN-driven T-cell lymphoma was sensitive to EZH2 degradation or CDK1 inhibition, which displayed synergy with US Food and Drug Administration\u2013approved histone deacetylase (HDAC) inhibitors.<\/jats:p>","DOI":"10.1182\/blood.2022016428","type":"journal-article","created":{"date-parts":[[2022,8,12]],"date-time":"2022-08-12T14:22:38Z","timestamp":1660314158000},"page":"2463-2476","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":22,"title":["Aberrant MYCN expression drives oncogenic hijacking of EZH2 as a transcriptional activator in\u00a0peripheral T-cell lymphoma"],"prefix":"10.1182","volume":"140","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0111-0263","authenticated-orcid":false,"given":"Marlies","family":"Vanden Bempt","sequence":"first","affiliation":[{"name":"1Laboratory for Experimental Hematology, Department of Oncology, KU Leuven, Leuven, Belgium"},{"name":"2Laboratory for the Molecular Biology of Leukemia, 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Leuven, Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kris","family":"Jacobs","sequence":"additional","affiliation":[{"name":"2Laboratory for the Molecular Biology of Leukemia, Center for Human Genetics, KU Leuven, Leuven, Belgium"},{"name":"3VIB- Katholieke Universiteit Leuven Center for Cancer Biology, Leuven, Belgium"},{"name":"4Leuvens Kanker Instituut, KU Leuven\u2013UZ Leuven, Leuven, Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olga","family":"Gielen","sequence":"additional","affiliation":[{"name":"2Laboratory for the Molecular Biology of Leukemia, Center for Human Genetics, KU Leuven, Leuven, Belgium"},{"name":"3VIB- Katholieke Universiteit Leuven Center for Cancer Biology, Leuven, Belgium"},{"name":"4Leuvens Kanker Instituut, KU Leuven\u2013UZ Leuven, Leuven, 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