Figure 1
From: Spontaneous loss of B lineage transcription factors leads to pre-B leukemia in Ebf1+/–Bcl-xLTg mice
Ebf1+/–Bcl-xLTg (EB) mice develop clonal lymphoproliferative disease. (a) Ebf1+/–Bcl-xLTg (EB) mice display ~50% penetrance of lymphoproliferative disease (LPD). Compared to control littermates (black dashed; Ebf1+/– and blue dashed; Bcl–xLTg), EB mice (red) developed clinical disease. At week 80, fractions of affected mice were 15/30 (EB), 1/21 (Bcl-xLTg) and 0/15 (Ebf1+/–). Affected mice displayed lethargy, hunched posture, enlarged lymph nodes and spleen. All aged Ebf1+/–and all but one Bcl–xLTg control littermates failed to develop clinical disease. P=0.0005 for EB vs Bcl–xLTg survival curves; Mantel–Cox test. N numbers given represent different mice of the indicated genotypes. (b–c) Comparison of spleens (b) and lymph nodes (c) from 1-year-old littermates: affected Ebf1+/–Bcl-xLTg (left), Bcl–xLTg control mouse (right). Spleen and lymph nodes from Ebf1+/– and wild-type control animals appeared similar to the Bcl–xLTg control shown. Representative of 15 EB, 20 Bcl–xLTg and 15 Ebf1+/– animals. (d–e) DNA was purified from affected Ebf1+/–Bcl-xLTg or control (Bcl-xLTg, WT) lymph nodes and PCR was used to detect VHJ558 or VH7183 immunoglobulin heavy chain rearrangements (d) and immunoglobulin lambda rearrangements (e). Each lane shows PCR product(s) from a different animal.
