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Fibroblast growth factor receptor 2 isoform IIIb (FGFR2b) is a transmembrane receptor tyrosine kinase and a specific splice variant of the FGFR2 gene. It is predominantly expressed in epithelial tissues, where it mediates essential mesenchymal-epithelial signaling during embryonic development and adult tissue repair [2, 12, 16]. The receptor is selectively activated by ligands such as FGF7, FGF10, and FGF22, triggering intracellular cascades including the MAPK and PI3K/AKT pathways to regulate cell proliferation, survival, and migration [2, 4, 13]. In various malignancies, particularly gastric and gastroesophageal junction adenocarcinomas, FGFR2b is frequently overexpressed or the FGFR2 gene is amplified, driving tumor progression and correlating with poor clinical outcomes [3, 8, 9]. Therapeutic targeting of FGFR2b involves monoclonal antibodies like bemarituzumab, which inhibit ligand binding and promote immune-mediated tumor cell death, as well as small-molecule inhibitors that block its kinase activity [2, 4, 15]. Clinical management often utilizes immunohistochemistry and genomic sequencing as biomarkers to identify patients likely to benefit from these targeted therapies [7, 9].
Inhibition of ligand binding; Antibody-dependent cell-mediated cytotoxicity (ADCC); Inhibition of tyrosine kinase activity
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