Recipient P-selectin and VCAM-1 are not required for engraftment of BCR-ABL1–expressing leukemic stem cells. (A) Kaplan-Meier survival curve for WT (B6129 F2, solid line, n = 33), VCAM-1 KO (Vcam1^flox/flox/TIE2Cre) mutant (dotted line, n = 5), or P-selectin KO (Selp^−/−) mutant (dashed line, n = 5) recipients of BCR-ABL1–transduced B6129 F2 BM. Here and in subsequent figures, the curve for the WT donor/recipient combination represents cumulative results from all transplants in this study. All mice that died prior to day 56 developed CML-like MPN. The difference in overall survival between the 3 cohorts was not significant (P = .81 for WT vs VCAM-1 KO and P = .96 for WT vs P-selectin KO; Mantel-Cox tests). (B) Increased clonality of CML-like disease in Vcam1 and Selp mutant recipients. Genomic DNA from spleen (spl) or PB of leukemic mice was analyzed by (upper) Southern blot with a GFP probe to detect distinct proviral integration events and (lower) subsequently with an ABL1 probe to allow determination of the total proviral content of each sample,³²  shown at the bottom. Con 1 and Con 2 are control DNAs from cell lines that each contain a single BCR-ABL1 provirus, whereas WT 1 and WT 2 are spleen DNA samples of WT recipients with BCR-ABL1–induced CML-like disease. Lanes 12 to 14 show the clonality of disease in P-selectin mutant recipients, whereas lanes 20 to 22 are representative leukemia samples from VCAM-1 mutant recipients.