Fig. 3. AML blasts exhibit a stable genotype and phenotype through treatment.

a DAb-seq performed on four bone marrow aspirates of a patient with AML during disease progression as indicated in the fishplot (black lines). The patient received multiple rounds of chemotherapy prior to the experiment (Supplementary Table 4). The fraction of blast cells with NPM1 W288Cfs*12 (NPM1^mut) mutation for each sampled timepoint detected by DAb-seq are shown in red. b Scatter plots with kernel densities show CD33 and CD34 signal for all cells (grey) and NPM1^mut cells (red) for each of the sampled timepoints. The percentages of normal and mutant cells within each gate are listed. Virtually gating cells highlights a persisting CD33⁺ blast population, which is eradicated with gemtuzumab, a CD33-targeted therapy. c UMAP embedding based on the log-transformed and corrected antibody counts from all cells labeled by timepoint indicates that the high-dimensional immunophenotype of the blasts is stable over the sampled timepoints. d The genotype of each cell at the NPM1 locus is plotted as a kernel density estimate using the UMAP coordinates from c. Antibody signals enriched among malignant and normal populations are plotted as kernel densities using all cells and labeled by genotype. Source data are provided as a Source data file.