Enforced BCL2 expression does not alter c-JUN–deficient leukemogenesis. (A) Protein levels of c-JUN and BCL2 in c-Jun^fl/fl and c-Jun^Δ/Δp185^BCR-ABL-transformed cells. β-ACTIN served as the loading control. (B) 1 × 10⁵ leukemic c-Jun^Δ/Δ B cells, transduced either with pMSCV-puro or pMSCV-Bcl2-puro, were injected IV into Rag2^−/− mice (n = 11 and n = 13, respectively; mean survival, 17 vs 17.5 days in mice injected with c-Jun^Δ/Δ-puro and c-Jun^Δ/Δ-Bcl2-puro cells, P = .3552) (top panel). Immunoblot analysis shows the enforced expression of BCL2 on a pMSCV-Bcl2-puro retrovirus infection in c-Jun^fl/fl and c-Jun^Δ/Δ cells. β-ACTIN served as the loading control (bottom panel). (C) Injection of c-Jun^fl/fl (n = 11) and c-Jun^fl/flCD19-Cre^+/− (n = 7) newborn mice with a replication-deficient Ab-MuLV–encoding retrovirus resulted in B-lymphoid leukemia/lymphoma (mean survival 31 vs 48 days in c-Jun^fl/fl and c-Jun^fl/flCD19-Cre^+/− mice, respectively, P = .0173). (D) Injection of c-Jun^wt/wt (n = 9) and c-Jun^AA/AA (n = 6) newborn mice with a replication-deficient Ab-MuLV–encoding retrovirus resulted in B-lymphoid leukemia/lymphoma (mean survival 52 vs 73 days in c-Jun^wt/wt and c-Jun^AA/AA mice, respectively, P = .6168).