FGF18 mediates fibroblast-leukemia cross talk to promote acute myeloid leukemia progression.
- Open access
FGF18 from stromal fibroblasts promotes AML progression by activating FGFR3 signaling and suppressing immune responses, with elevated levels linked to poor prognosis.
- Why it matters: Understanding stromal contributions to leukemia progression and immune evasion is crucial for developing targeted therapies, as these interactions are poorly characterized in AML.
- What they did: The study used single-cell RNA sequencing, genetic depletion, and CRISPR-Cas9 screens to identify FGF18's role in AML, revealing its interaction with FGFR3 and downstream signaling pathways.
- The result: Blocking FGF18 with a neutralizing antibody disrupted leukemia-stroma crosstalk, restored immune function, and enhanced anti-PD-1 therapy, suggesting a promising therapeutic approach.