Abstract
The Eµ-TCL1 transgenic mouse model represents the most widely and extensively used animal model for chronic lymphocytic leukemia (CLL). In this report, we performed a meta-analysis of leukemia progression in over 300 individual Eµ-TCL1 transgenic mice and discovered a significantly accelerated disease progression in females compared to males. This difference is also reflected in an aggressive CLL mouse model with additional deletion of Tp53 besides the TCL1 transgene. Moreover, after serial adoptive transplantation of murine CLL cells, female recipients also succumbed to CLL earlier than male recipients. This sex-related disparity in the murine models is markedly contradictory to the human CLL condition. Thus, due to our observation we urge both careful consideration in the experimental design and accurate description of the Eµ-TCL1 transgenic cohorts in future studies.
Highlights
Increasing understanding of the biology and pathogenesis of chronic lymphocytic leukemia (CLL) has led to many breakthroughs in the treatment of this disease [1,2], which has been acquired owing considerably to the use of animal models
All analyzed mice were hemizygote for the T cell leukemia 1 (TCL1) transgene (Eμ-TCL1tg/wt ), had either a hybrid C3H/HeJ × C57BL/6 (B6C3) or a C57BL/6 (B6) genetic background, and were housed in groups of up to five animals per cage in individually ventilated cages (IVC) in three different animal facilities of the University Hospital of Cologne (Table 1)
Mice housed in the Institute of Experimental Medicine (EM) and the Institute of Pathology (PA) were specific pathogen-free (SPF), mice housed in the facility of the CECAD Research Center were specific and opportunistic pathogen-free (SOPF)
Summary
Increasing understanding of the biology and pathogenesis of chronic lymphocytic leukemia (CLL) has led to many breakthroughs in the treatment of this disease [1,2], which has been acquired owing considerably to the use of animal models. The ectopic expression of the human T cell leukemia 1 (TCL1) oncogene under the control of the VH -promoter and IgH -Eμ-enhancer in transgenic mice enables the development of a highly similar CLL-like disease with 100% penetrance. Cancers 2020, 12, 1980 a pre-clinical model for different treatment options [4,5,6,7] Given their intensive usage, a thorough understanding of CLL pathogenesis in Eμ-TCL1 transgenic mice is critical for the precise interpretation of the acquired results.
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