At this age, Eμ-TCL1 mice presented a slightly enlarged spleen and a much higher cellularity in the peritoneal cavity, ranging between 50- to 100-fold increase. The cell cycle distribution and the rate of cell proliferation in spleen and peritoneal cavity of these transgenic mice were also investigated and we found that IgM+CD5+ sorted populations were arrested in the G0/G1 phase of the cell cycle and did not actively divide. The onset of a frank leukemia in the elderly mice provided the final evidence of the establishment of a murine model for human CLL [21, 31]. All mice between 10 and 20 months of age became visibly ill and presented with spleno- and hepatomegaly associated with high counts of white blood cells (WBCs). Moreover, some mice also developed advanced lympho-adenopathy, another hallmark of human CLL [21, 31]. Simultaneously, another Tcl1 transgenic mouse model was created to express Tcl1 in both, B- and T-cells [49]. The phenotype of CLL like disease in this second mouse was similar to that described for our Tcl1 transgenics.
