Fig. 1: The Eµ-myc mouse lymphoma model recapitulates molecular signatures and some clinical features of human DLBCL.
From: H3K9me3-mediated epigenetic regulation of senescence in mice predicts outcome of lymphoma patients

a Utilization of the Eµ-myc model in a clinical trial-like fashion. Eµ-myc lymphomas were transplanted into wild-type recipients and treated with CTX upon lymphoma formation. After initial remission, tumors that relapsed (RP, unlike those that did not [NR]) were retreated. Lymphomas were considered clinically resistant after a third relapse (RES). b Tumor-free survival of CTX-treated mice after first(-line) treatment (n = 76, green line), after second treatment (n = 31, blue line), and after third treatment (n = 28, red line). Two mice per lymphoma were monitored for response. c Principal components analysis based on signature genes separating patients with Burkitt’s lymphoma (n = 98) from those with DLBCL (n = 1305) in different datasets and Eµ-myc lymphomas (n = 154). Each dataset was separately row (gene) mean-centered and scaled to unit variance before being combined in a single dataset. The larger white-bordered points denote the centroid of each lymphoma type. d Tumor-free survival of CTX-treated mice bearing ABC-like (n = 10), GCB-like (n = 24) or unclassified (n = 42) Eµ-myc lymphomas. Two mice per lymphoma were used. e Pattern comparison of multiple GSEA results of the three distinct CCC subgroups (as indicated) with one compared against the two others for DLBCL cases and Eµ-myc lymphomas. Each column shows group-specific upregulated gene sets. The color code denotes analyses of each CCC group against the rest. NES normalized enrichment score.