TET2 deficiency reprograms the germinal center B cell epigenome and silences genes linked to lymphomagenesis.

GSEA analysis on this Aicda -associated promoter gene set in Tet2 −/− GC B cells indicated a significant trend for these genes to be expressed at lower levels in Tet2 −/− GC B cells (FDR = 0.037; Fig. 5C ).

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In addition, running GSEA in the opposite direction, that is, testing of 614 murine Tet2 −/− hypermethylated genes in the expression data in human TET2 mutant versus WT DLBCLs, showed a trend toward negative regulation of the murine Tet2- deficient gene signature in human DLBCLs (NES = −1.12, FDR = 0.53; Fig. 7B ).

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This procedure yielded highly significant enrichment for genes induced in centrocytes as they exit the GC reaction, CD40-induced genes, and genes involved in antigen presentation ( Fig. 3A and table S4).

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