fig1

Figure 1. Schematic representation of the EGFR signaling axis and its most important downstream targets in the AML microenvironment. EGFR ligands in the bone marrow microenvironment phosphorylate EGFR receptors on the surface of LSPC or CD8⁺ T cells, leading to the production and release of IL-3. In turn, IL-3 induces proliferation signals in LSPCs, promoting the expansion of AML cells. Direct arrows represent direct interactions, and the dotted arrow represents indirect effects. AML: Acute myeloid leukemia; LSPCs: leukemia stem/progenitor cells; IL-3: interleukin-3; EGFR: epidermal growth factor receptor; EGF: epidermal growth factor; TGF-α: transforming growth factor-alpha; AREG: amphiregulin; HB-EGF: EGF-like heparin-binding factor; BTC: betacellulin; EPR: epiregulin; SFK: src family kinases; PI3K: phosphatidylinositol 3-kinase; AKT: protein kinase B; JAK2: Janus-activated kinase 2; JAK: Janus-activated kinase; STAT5: signal transducer and activator of transcription 5. Image created using BioRender.com.