Fig. 2

TCP and TCA mice develop a CLL-like disease. Conditional B cell-specific deletion of Trp53 and Atm in TCL1-driven murine CLL leads to the development of a disease displaying morphological and histological features, as well as surface marker profiles consistent with a CLL-like disease. a H/E stainings of spleens, lymph nodes, bone marrow, and blood smears of TC, TCA, and TCP mice and WT controls. Scale bars overview: 200 µm; scale bars inserts: 25 µm. b Representative H/E and Ki67 stainings of spleens isolated from animals with CLL-like and transformed disease (RS Richter’s syndrome). Lymphomas of Myd88 ^{condp.L252P/wt} ;R26 ^LSL.BCL2/wt ;Cd19 ^{Cre/wt 22} and EµTCL1;Cd19 ^Cre/wt ;AKT ^C (Al-Maarri et al., unpublished) were included as an internal reference. Scale bars overview: 50 µm; scale bars inserts: 20 µm. c Quantification of the Ki67 stainings from untransformed and transformed animals (n = 5 for TC, TCA, and TCP, n = 3 for RS cases). d Quantification of the frequency of Richter transformation in the different mouse lines (TC: n = 23, TCP: n = 18, TCA: n = 7). e Blood smears of a TCP animal before (age = 20 weeks) and after transformation (age = 28 weeks) show the appearance of large blastoid cells in the peripheral blood upon transformation. Scale bars: 20 µm. The appearance of these large cells was accompanied by the loss of CD5 expression of the leukemic clone in the peripheral blood, illustrated in f. Error bars represent standard deviation. Welch’s t-test, ***p ≤ 0.001