Leukemic granulocytes or progenitors do not initiate or enhance the CML-like disease. Hematopoietic subpopulations were isolated by FACS sorting from BM of 3-week-induced leukemic SCLtTA/BCR-ABL (dtg) and wt or stg control mice. Purification of cell populations was performed according to surface markers expressed by LSK cells, progenitors (Lin⁻Sca-1⁻c-kit⁺), or granulocytes (Gr-1⁺CD11b⁺). Recipients were transplanted with 1 × 10⁶ ufBM, 2500 LSK cells, 2500 progenitors, or 3.6 × 10⁵ granulocytes. In addition, LSK cells were added back to additional groups of mice receiving granulocytes or progenitors. Each error bar represents the mean ± SD. (A) The percentage of immature granulocytes (Gr-1^low/CD11b⁺) measured in BM and spleen of mice transplanted with different subpopulations of cells. (B) Spleen weight was unchanged in mice receiving granulocytes or progenitors only. (C) Histologic analyses of spleen were performed by NACE stain. Infiltration with granulocytes and disturbed follicles were only evident in spleens of recipients transplanted with ufBM, LSK cells, or LSK cells added back to granulocytes or progenitors. Slides are depicted at original magnifications of ×10 or ×20. Mice receiving ufBM, LSK, progenitors, or LSK⁺ progenitors isolated from stg or dtg mice were analyzed between 49 to 55 days after transplantation. Mice receiving granulocytes from dtg or stg donors were analyzed 77 days after transplantation. Recipients of dtg LSK cells or LSK cells plus granulocytes were analyzed 126 days after transplantation. n = 4 each for ufBM, LSK, progenitors, or Gr1⁺CD11b⁺ cells. n = 4 (stg) or 3 (dtg) for LSK⁺ progenitors; n = 3 dtg for LSK and LSK+ Gr1⁺CD11b⁺ cells. *P < .05.