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As functional consequences of <jats:italic>ZNF217<\/jats:italic> alterations remain unknown, we comprehensively evaluated their impact in PMBCL. Targeted sequencing identified genetic lesions affecting <jats:italic>ZNF217<\/jats:italic> in 33% of 157 PMBCL patients. Subsequent gene expression profiling (<jats:italic>n<\/jats:italic>\u2009=\u2009120) revealed changes in cytokine and interferon signal transduction in <jats:italic>ZNF217<\/jats:italic>-aberrant PMBCL cases. In vitro, knockout of <jats:italic>ZNF217<\/jats:italic> led to changes in chromatin accessibility interfering with binding motifs for crucial lymphoma-associated transcription factors. This led to disturbed expression of interferon-responsive and inflammation-associated genes, altered cell behavior, and aberrant differentiation. Mass spectrometry demonstrates that ZNF217 acts within a histone modifier complex containing LSD1, CoREST and HDAC and interferes with H3K4 methylation and H3K27 acetylation. Concluding, our data suggest non-catalytic activity of ZNF217, which directs histone modifier complex function and controls B cell differentiation-associated patterns of chromatin structure.<\/jats:p>","DOI":"10.1038\/s41375-023-02013-9","type":"journal-article","created":{"date-parts":[[2023,8,30]],"date-time":"2023-08-30T09:02:50Z","timestamp":1693386170000},"page":"2237-2249","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Frequent ZNF217 mutations lead to transcriptional deregulation of interferon signal transduction via altered chromatin accessibility in B cell 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