MMP-9 deficiency impaired the development of CML-BC–like disease induced by BCR-ABL and Hes1 in mouse BMT models. (A) Kaplan-Meier analysis for the survival of mice that received transplants of WT or MMP-9–deficient CMPs transduced with the combination of BCR-ABL and Hes1. The numbers of transplanted mice are shown. Statistically significant differences were observed in latency and penetrance (log-rank test, P = .000146). (B-D) The morbid mice transplanted with WT or MMP-9–deficient CMPs expressing BCR-ABL and Hes1 were used. (B) Cytospin preparations of BM cells were stained with Giemsa. A representative photo is shown. Images were obtained with a BX51 microscope and a DP12 camera (Olympus); original magnification ×100. (C) Blast ratios in the BM. The mean blast ratios in all nucleated BM cells were 39.3% ± 9.7% and 35.1% ± 8.9% in mice receiving WT or MMP-9–deficient CMPs transduced with the combination of Hes1 and BCR-ABL, respectively (2-sample Student t test with Welch correction, P = .289). (D) Flow cytometric analysis of BM cells. The dot plots show Gr-1, CD11b, B220, CD3, CD4, CD8a, c-Kit, Sca-1, and CD34 labeled with the corresponding phycoerythrin-conjugated mAb vs expression of GFP. GFP is a marker of BCR-ABL transduction.