Lack of P-selectin and ICAM1 accelerates the development of CML-like leukemia induced by BCR/ABL (A) Kaplan-Meier survival curve for recipients of marrow transduced by BCR/ABL. Recipient mice received a cell dose of 1 × 10⁵ cells/mouse. There were significant differences in survival between wild-type (WT) recipients of transduced WT marrow and P-selectin/ICAM1-deficient recipients of transduced P-selectin/ICAM1-deficient marrow (P = .001, log-rank test). (B) Mean spleen weight (mean values ± SD) of leukemic mice (measured at the time of morbidity or death). There was no significant difference in spleen weight between the 2 transplant groups (P = .363, t test). (C) Bone marrow colony formation assay. Bone marrow cells from wild-type and P-selectin^-/-/ICAM1^-/- mice were transduced with MSCV-P210-IRES-GFP or the parental control (MSCV-IRES-GFP) retrovirus, and the transduced cells were assayed for colony formation. The average number of colonies (mean values ± SD) from triplicate platings was determined in the absence or presence of 100 pg/mL murine IL-3. (D) Pathological analysis (hematoxylin/eosin staining) of the lungs and spleens of CML mice at the time of morbidity and death. In the normal control group, nontransduced wild-type bone marrow cells were transplanted into lethally irradiated wild-type recipient mice. In contrast to normal control mice, BCR/ABL-transduced WT to WT and P-selectin^-/-/ICAM1^-/- to P-selectin^-/-/ICAM1^-/- transplant groups showed complete infiltration of the lungs with myeloid leukemic cells and severe lung hemorrhages; P-selectin^-/-/ICAM1^-/- to P-selectin^-/-/ICAM1^-/- transplant mice showed more severe and larger areas of lung hemorrhages. In contrast to the normal control group, BCR/ABL-transduced WT to WT and P-selectin^-/-/ICAM1^-/- to P-selectin^-/-/ICAM1^-/- transplant groups demonstrated complete disruption of follicular architecture of the spleen by infiltrating myeloid leukemic cells.