Suppression of Bcr-Abl/ΔSH2–induced B-lymphoproliferative disorder by Bcr-Abl–induced MPD.

(A) Lethally irradiated recipient mice were transplanted with a mixture of mock-transduced, bcr-abl–transduced, andbcr-abl/ΔSH2–transduced BM cells at the ratio as indicated. (B) WBCs were shown for 4 1:4 mix BMT mice (column 1), 5 1:8 mix BMT mice (column 2), and 9 Bcr-Abl/ΔSH2 BMT (column 3) on day 22 after BMT. The total numbers of B-lymphoid cells (CD19⁺) in 1:4 mix BMT mice (column 4), 1:8 mix BMT mice (column 5), and Bcr-Abl/ΔSH2 mice (column 6) are calculated as in Figure 4. (C) Genomic DNAs of PB cells from Bcr-Abl mouse (lane 1), 1:4 mix BMT mice (lanes 2-5), 1:8 mix BMT mice (lanes 6-10), and Bcr-Abl/ΔSH2 mouse (lane 11) were digested with restriction enzyme HindIII and subjected to Southern blot analysis with a ³²P-labeled 1.2-kb Eco47III-BglII fragment from 3′ end of human c-abl gene. Sizes of DNA fragments from thebcr-abl (4.6 kb) and bcr-abl/ΔSH2 (4.3 kb) genes are labeled. The percentage of bcr-abl andbcr-abl/ΔSH2 cells (represented by the intensity ofbcr-abl and bcr-abl/ΔSH2 bands) in total infected cells (represented by the sum of intensity ofbcr-abl and bcr-abl/ΔSH2 bands) are shown. Also shown are the total WBC counts and the percentages of GFP⁺WBC, B cells, and GFP⁺ B cells in PB at the time when the DNA was made. The percentage values above 10% were shown as integers; values below 10% were rounded to the first decimal.