Fig. 2: NK cell phenotype changes to more mature during the TKI treatment.

a UMAP representation of the NK CD16 + , NK CD16-, and NK cells identified by Celltypist, colored by manually annotated clusters or scaled expression of genes used to annotate the phenotypes. b Scaled average expressions (avg exp) and proportion of cells expressing (pct.exp) the canonical markers used to define the clusters. Encircled dots are differentially expressed (P_adj < 0.05, Bonferroni corrected t-test) in a given cluster in comparison to other clusters. c Top: The number of NK cells from each condition. Bottom: The median proportion of NK cell subtypes out of total NK cells within each condition. Colors in the lower panel map to UMAP colors in a. d ScRNAseq population abundances in patients with CML (diagnosis n = 4, on TKI n = 6, N = 6, off TKI n = 6, N = 10) and healthy controls (n = 7). P-values were calculated with a two-sided Mann-Whitney test. e Left: Differentially expressed genes (P_adj < 0.05, Bonferroni corrected t-test) in active CD56^dim NK cells (cluster 0) from before TKI cessation between patients who sustain treatment-free remission (TFR) and patients who had early relapse ( < 6 months) after cessation. Right: Cytotoxicity score of active CD56^dim NK cells (cluster 0) in baseline in patients who sustain TFR and early relapse. Note that multiple genes upregulated in patients with early relapse were associated with cytotoxicity. f Left: Differentially expressed genes (P_adj < 0.05, Bonferroni corrected t-test) in active CD56^dim NK cells (cluster 0) from after and before TKI cessation, separately in TFR and early relapse. CML=chronic myeloid leukemia, CLL = chronic lymphocytic leukemia, AML= acute myeloid leukemia, RCC = renal cell carcinoma, NSCLC = non-small cell lung carcinoma, TKI = tyrosine kinase inhibitor. N refers to the number of patients and N to the number of samples where it differs from n. *=P < 0.05, **=P < 0.01, ***=P < 0.001, ****=P < 0.0001.