Fig. 4: Myeloid leukemia growth and propagation depend on Syndecan-1.

a Approach to assess the impact of Sdc1 deletion on bcCML. b Sdc1 in WT and Sdc1^−/− bcCML (blue/DAPI, green/Msi2, red/Sdc1; 63x). c Colony formation of WT and Sdc1^−/− bcCML. **P = 0.002 primary and ***P = 0.0001 secondary (n = 3 technical replicates from four biological replicates). d Limiting dilution assay of WT and Sdc1^−/− bcCML (LEFT). ****P < 0.0001 (n = 3 technical replicates from one biological replicate for WT, n = 6 technical replicates from two biological replicates for Sdc1^−/−). Extreme limiting dilution analysis (RIGHT). Stem cell frequency: WT 1/1, Sdc1^−/− 1/94, ***P = 0.0002. e Representative chimerism in mice transplanted with WT or Sdc1^−/− bcCML. ***P = 0.0007 (n = 3 for WT and n = 4 for Sdc1^−/−). f Intrafemoral transplant of WT or Sdc1^−/− bcCML. *P < 0.03 (n = 3 mice for each cohort). g Survival curves for WT or Sdc1^−/− bcCML. *P = 0.01 (n = 5 each cohort). h Imatinib response in WT and Sdc1^−/− bcCML. Significance from 0 μM: WT ***P = 0.0001, ****P < 0.0001; Sdc1^−/− **P = 0.004, ***P = 0.0004 (% is relative to 0 μM for each group, n = 3 technical replicates). i Ectopic expression of Sdc1/HS-null Sdc1 in Sdc1^−/− bcCML. *P = 0.01, **P = 0.002 (n = 3 technical replicates from three biological replicates). Two-tailed unpaired Student’s t-tests were used to determine statistical significance. Source data are provided as a Source Data File.