fig1
Figure 1. Genomic architecture and clonal evolution of AML. Schematic illustrating the progression from normal hematopoietic stem cells (HSCs) to pre-leukemic HSCs (pHSCs) via clonal hematopoiesis (CH) mutations (DNMT3A, TET2, ASXL1, KMT2D, TP53), followed by overt AML defined by 11-13 molecular subgroups (e.g., NPM1 mutations, RUNX1-RUNX1T1, CBFB-MYH11, KMT2A rearrangements, TP53/aneuploidy, spliceosome/cohesin clusters). Right panel depicts archetypal evolutionary patterns (linear, branching, de novo from pHSCs) with resistance mutations (e.g., FLT3 Phe691Leu, BCL2 Gly101Val) and serial NGS monitoring timepoints per ELN 2022 guidelines. Figure generated using AI-based tools and finalized by the authors in Microsoft PowerPoint. AML: Acute myeloid leukemia; NGS: next-generation sequencing; AI: artificial intelligence.







