Effect of overexpression of Bcl-xL on cell-cycle entry and response to antineoplastic treatment. (A) Schematic of hBcl-xL transgene. TRE is the responsive element with minimal promoter upstream of the human Bcl-x_L cDNA followed by intervening sequence (IVS) and poly A site. (B) Graph displaying difference in B220^dim/CD⁺ S + G₂M status in splenocytes isolated from MMTV hbcl-xL and littermate controls (WT; mean ± SEM). For wild-type, n = 5; MMTV hbcl-xL, n = 3. * indicates statistically significant; and **, statistically highly significant. (C) Splenocytes from B-ALL and hbcl-xL B-ALL mice were isolated 16 hours after BrdU injection. Cells were stained with fluorescently labeled antibodies to B220, CD19, and BrdU. Cell-cycle analysis, BrdU versus 7-AAD, is shown for the B220^dim/CD19⁺ population. (D) Western blot analysis of protein lysates from the spleen of B-ALL (lanes 1 and 2), hbcl-xL B-ALL (lanes 3 and 4), and Bcl-x–deficient B-ALL diseased mice. (E) Percentage of cells undergoing apoptosis in bone marrow and spleen after treatment with cyclophosphamide. Animals were killed after a single administration of the drug (results are given as mean ± SEM; n = 3).