IκBαSR expression prolongs survival of mice with BCR-ABL1–induced B-ALL. (A) Kaplan-Meier survival curve for recipients of BCR-ABL1/GFP– or BCR-ABL1/IκBαSR–transduced BM. The number of individual mice in each arm is indicated; all mice developed B-ALL. Mice with B-ALL induced by the BCR-ABL1/IκBαSR retrovirus survived significantly longer than control (P = .0096, Mantel-Cox test). (B) Genomic DNA from pleural effusion lymphoblasts of B-ALL mice was subjected to Southern blot analysis to quantify leukemia-initiating cells, as described in “Materials and methods.” The difference in number of proviral clones between leukemias induced by BCR-ABL1/GFP (lanes 1-10, 8.1 ± 3.5 independent clones) or BCR-ABL1/IκBαSR (lanes 11-22, 5.8 ± 2.0 independent clones) was of borderline significance (P = .0697, Student t test). The 2 control DNAs (Con, lanes 23-24) were from cell lines that each contained a single BCR-ABL1 provirus. The same blot was reprobed with a human ABL1 probe to calculate the total proviral copy number per genome, as described.²¹