{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nIn a wide spectrum of solid tumors, PDGFRA is increasingly recognized as a pivotal oncogenic driver. In glioblastoma multiforme and pediatric high‐grade gliomas, aberrant PDGFRA activation—whether by amplification, gene rearrangements, or point mutations—helps define distinct molecular subtypes that correlate with tumor heterogeneity and differential responses to aggressive therapy. Similarly, in gastrointestinal stromal tumors (GISTs) PDGFRA mutations represent an alternative, mutually exclusive mechanism to KIT activation. Specific PDGFRA variants not only influence tumor behavior and malignant potential but also determine sensitivity or resistance to receptor‐targeted therapies such as imatinib and sunitinib. In addition, PDGFRA activation can occur via intragenic deletions or fusion events that confer constitutive kinase activity and further drive oncogenic signaling through downstream effectors including the PI3K, MAPK, and Src pathways."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "29"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn hematologic disorders and infectious contexts, abnormal PDGFRA activity also plays a critical role. Rearrangements such as the FIP1L1‐PDGFRA fusion result in constitutive receptor activation and are found in a subset of patients with idiopathic hypereosinophilic syndrome and systemic mast cell disease, conferring exquisite sensitivity to tyrosine kinase inhibitors like imatinib. Moreover, PDGFRA has been implicated in rare cases of acute myeloid leukemia and T‐cell lymphoblastic lymphoma, and functional studies reveal its importance in mediating viral entry—for example, human cytomegalovirus exploits PDGFRA to trigger downstream PI3K–Akt signaling, underscoring its relevance in both neoplastic and infectious processes."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "30", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its role in oncogenesis and hematologic malignancies, PDGFRA is instrumental in normal development, tissue maintenance, and repair. PDGFRA signaling critically regulates progenitor cell proliferation and fate decisions in the central nervous system—guiding oligodendrocyte differentiation—as well as in mesenchymal stem cell niches in the bone marrow and cardiac compartments. This receptor also influences fibrotic remodeling in multiple organs, including the kidney, gastrointestinal tract, and white adipose tissue, where PDGFRA‐positive progenitors may shift toward a fibrogenic phenotype under pathological conditions. In parallel, regulatory networks involving microRNAs modulate PDGFRA expression in endothelial cells, further linking its activity to angiogenesis and tissue remodeling. Such multifunctionality in both physiologic and pathologic contexts makes PDGFRA an attractive target for novel therapeutic strategies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "36", "end_ref": "49"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Michael C Heinrich, Christopher L Corless, Anette Duensing, et al. 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