{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNTRK3 is a member of the neurotrophin receptor family that normally binds neurotrophin‐3 (NT‑3) to regulate cell survival, differentiation, and proper neuronal development. In the presence of NT‑3, NTRK3 activates downstream cascades such as Ras–MAPK and PI3K–Akt to promote cell survival and differentiation, whereas in the absence of its ligand it acts as a “dependence receptor” that induces apoptosis. This conditional behavior has important implications in tumor biology; for example, epigenetic silencing or aberrant methylation of NTRK3 can abrogate its tumor‐suppressive function in colorectal cancers, thereby permitting neoplastic transformation and progression."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAlternatively, rearrangements that fuse NTRK3 with 5′ partner genes—most notably the recurrent ETV6–NTRK3 fusion—yield chimeric proteins that possess potent, ligand‐independent tyrosine kinase activity. The resultant constitutive activation drives oncogenic transformation by robustly stimulating mitogenic signaling pathways while preserving the capacity for epithelial differentiation. Such fusions have been identified as primary oncogenic events in secretory breast carcinoma, mammary analogue secretory carcinoma of salivary gland, certain thyroid neoplasms, pediatric fibrosarcoma, and even in subsets of gastrointestinal stromal tumors, underscoring the diverse tumor types in which the aberrant NTRK3 kinase domain plays a critical role."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "3", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its direct role in oncogenesis, alterations in NTRK3 are proving valuable as diagnostic markers and therapeutic targets. Sensitive detection methods—such as pan‐TRK immunohistochemistry—can screen for NTRK3 fusions across a range of tumor types, thereby guiding the application of selective TRK inhibitors. Moreover, beyond its fusion‐driven oncogenic role, differential expression of NTRK3 has been linked to prognostic outcomes in tumors such as medulloblastoma (with higher TrkC expression correlating with longer survival) and to genetic susceptibility in neuropsychiatric conditions including obsessive–compulsive hoarding and schizophrenia. Additional studies have highlighted that noncoding RNAs may modulate NTRK3 expression and thereby influence tumor cell invasion and migration, while somatic point mutations in NTRK3 have been reported in various malignancies, further underscoring its multifaceted role in both normal development and disease pathogenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Anne-Laure Genevois, Gabriel Ichim, Marie-May Coissieux, et al. 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