Expression of IκBαSR attenuates CML-like MPN induced by BCR-ABL1. (A) Kaplan-Meier survival curve for CML-like MPN induced by BCR-ABL1/GFP or BCR-ABL1/IκBαSR. The number of individual mice in each arm is indicated. All mice receiving BCR-ABL1/GFP–transduced BM developed CML-like MPN; recipients of BCR-ABL1/IκBαSR–transduced BM developed CML-like MPN (▪) except for 1 recipient who developed B-ALL (□), and had significantly longer survival than recipients of BCR-ABL1/GFP–transduced BM (P < .0001, Mantel-Cox test). (B) Analysis of leukemia-initiating cell frequency in recipients from the 2 cohorts in panel A. Leukemias induced by BCR-ABL1/GFP (lanes 1-11) had a significantly higher number of independent clones (9.9 ± 2.8) than leukemias induced by BCR-ABL1/IκBαSR (lanes 12-19; 6.8 ± 1.4 clones, P = .0096, Student t test). The control DNA (C, lane 20) was from a cell line that each contained a single BCR-ABL1 provirus. (C) Immunoblot of protein lysates from spleens of mice with CML-like MPN induced by BCR-ABL1/GFP (lanes 2-3) or BCR-ABL1/IκBαSR (lanes 4-5) with the indicated antibodies. Lysate from untransduced mouse BM (lane 1) served as a control. The relative expression of c-MYC was quantified and normalized to actin (bar graph).