Figure 7.

AML mosaic integration bridges RNA, protein, and genotype across independent cohorts. (A) Joint latent UMAP colored by data set/modality (AML CITE RNA/ADT, van Galen RNA, DAb-seq ADT). (B) Joint UMAP highlighting DAb-seq NPM1 status (WT/MUT; unlabeled gray). (C) k-NN probability transfer of NPM1 from van Galen → DAb-seq (k = 60), shown on DAb-seq cells. (D) Joint UMAP colored by van Galen cell-state labels. (E) Joint UMAP colored by van Galen NPM1 status for labeled cells. (F) k-NN probability transfer of NPM1 from DAb-seq → van Galen (k = 50), shown on van Galen cells. (G) Refined UMAP colored by van Galen cell-state labels. (H) Joint UMAP after mutation-head refinement (encoders fine-tuned; decoders frozen), colored by data set/modality. (I) Refined UMAP colored by LSC17 stemness score. (J) Refined UMAP colored by DAb-seq NPM1 status. (K) Refined UMAP colored by van Galen NPM1 status (labeled cells only). (L) Mutation-head test performance (AUC) across recurrent AML genes in DAb-seq and van Galen (genes with insufficient labeled test cells omitted/NA).

2068f07