Figure 1.
Mouse models develop clonal DLBCL-like disease. (A) Schematic visualizations of the alleles used throughout the manuscript. Triangular shapes represent loxP sites. (B) Survival was determined for both the Prdm1-proficient (MBC/79-MBC) and Prdm1-deficient (PPMBC/79-PPMBC) models. (C) Representative MRI images of overt lymphoma in the 4 mouse lines; L, lymphoma; S, spleen; and K, kidney. (D) Representative immunohistochemical stainings of lymphoma tissue isolated from MBC, 79-MBC, PPMBC, and 79-PPMBC animals. (E) Quantification of the terminal phenotypes as determined by macroscopic and histological/immunohistochemical analysis; int, intestinal. (F) Quantification of the frequency of Ki67+ cells in lymphoma sections from the indicated genotypes. Each data point represents a lesion from an individual animal. (G-I) BCR sequencing was performed on cDNA of lesions histologically characterized as tumors and PNA+ GCB cells from wildtype animals. (G) shows representative clonality plots of 1 sample per genotype. Within each sample, each circle represents a unique BCR sequence, whereas the size of the circle represents the frequency of this sequence within the sample. Sequences differing by a maximum of 2 nucleotides are considered to be clonally related and therefore connected to clones by connecting lines. The dominant clone of each sample is highlighted in blue. The size of the largest clone of each analyzed sample (PNA+ B, n = 4; MBC, n = 8; 79-MBC, n = 10; PPMBC, n = 5; and 79-PPMBC, n = 6) is plotted in panel H and the identified heavy chains are quantified in panel I; ∗P ≤ .05; Welch 2-tailed t test, Benjamini-Hochberg-correction for multihypothesis testing. cDNA, complementary DNA; PNA, peanut agglutinin.