Phospholipase C and Ca⁺⁺ signaling is enriched in AML1-ETO transformed LSCs. (A) Outline of the proteomic workflow. (B) Gene set enrichment analysis (GSEA) on murine MLL-AF9 (MLL9) and AML1-ETO (AE) LSCs (n = 4 per genotype). (C) Ingenuity pathway analysis (IPA) on murine AML1-ETO transformed LSC compared with MLL-AF9 positive controls. (D) Schematic of proteome analysis of primary human AML1-ETO/t(8;21) AML (n = 4 per genotype). (E) Molecular analysis of AML patient samples applied for proteomic analysis. (F) GSEA on human t(8;21) AML compared with non-t(8;21) controls. (G) t-SNE plot displaying the gene expression landscape of 641 AML patients of the HOVON cohort¹⁹ with an overlay of different AML subtypes (left) with absolute PLCG1 expression values (right). (H) PLCG1 protein expression in AML1-ETO positive (Kasumi-1, SKNO-1) vs AML1-ETO⁻ human AML cell lines analyzed by intracellular flow cytometry (n = 5 per cell line; 1-way analysis of variance [ANOVA]). (I) Relapse-free survival (RFS, B) in patients with t(8;21) AML according to the expression level of PLCG1. Survival curves were estimated with the Kaplan-Meier method and compared using a log-rank test. (J) Scatterplot depicting PLCG1 expression levels in t(8;21) patients according to their relapse status (no relapse, n = 33; relapse, n = 27; unknown, n = 2).