[Pathogenic mechanisms and targeted therapeutic advances of the FGF/FGFR signaling pathway in hematological malignancies].

The signaling axis composed of fibroblast growth factors (FGFs) and fibroblast growth factor receptors (FGFRs) is a core regulatory hub for the morphogenesis and homeostatic maintenance of the hematopoietic system. Accumulating evidence indicates that aberrant activation of the FGF/FGFR signaling axis contributes to malignant progression, bone marrow microenvironment remodeling, and chemoresistance in hematological malignancies. At the molecular level, the principal pathogenic mechanism involves oncogenic fusion proteins generated by chromosomal translocations; these proteins drive constitutive kinase activation, with the ZMYM2-FGFR1 fusion gene as a classic example. At the cellular level, this signaling axis remodels the bone marrow microenvironment via paracrine signaling, thereby inhibiting apoptosis and inducing a microenvironment-mediated multidrug resistance phenotype. Agents that precisely target and block the FGF/FGFR signaling network-such as selective FGFR inhibitors, dual FLT3/FGFR kinase inhibitors, and the small-molecule FGF trap NSC12-represent promising therapeutic strategies for hematological malignancies. This review summarizes the mechanisms through which FGF/FGFR signaling contributes to common hematological malignancies, including myeloid malignancies, multiple myeloma, T-cell acute lymphoblastic leukemia, and B-cell lymphoma, and discusses the potential of targeting this pathway for clinical intervention. These insights may help guide the application of FGF/FGFR-targeted strategies in hematological malignancies.