{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSTAT6 is a pivotal transcription factor activated downstream of interleukin‑4 (IL‑4) and interleukin‑13 (IL‑13) that orchestrates multiple facets of immune regulation. In diverse immune cells—such as T helper cells, dendritic cells, and macrophages—STAT6 mediates gene transcription programs essential for Th2 differentiation, allergic inflammation, and epithelial barrier function. By recruiting coactivators (for example, the p100 bridging protein) and promoting chromatin modifications, STAT6 facilitates the induction of key mediators including cytokines, chemokines, mucins, and other epithelial products. Its rapid phosphorylation and nuclear translocation underscore a role in fine‑tuning responses ranging from immunoglobulin E regulation to the suppression of pro‑inflammatory pathways."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the realm of tumorigenesis—particularly in solitary fibrous tumors (SFTs)—STAT6 assumes a unique oncogenic role via recurrent gene fusions with NAB2. These NAB2‑STAT6 fusions convert a transcriptional repressor into an aberrant activator, resulting in the constant nuclear localization of STAT6 that is both highly sensitive and specific as a diagnostic marker for SFT. Moreover, the spectrum of fusion variants correlates with distinct histologic patterns and clinical behaviors, underscoring STAT6‑driven transcriptional deregulation as a defining event in the pathogenesis of these mesenchymal neoplasms."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "22"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond SFTs, aberrations in STAT6—through activating mutations, altered expression, or gene amplification—have been implicated in a variety of hematologic and solid tumors. In lymphomas such as primary mediastinal B‑cell lymphoma and follicular lymphoma, as well as in colorectal and prostate cancers, dysregulated STAT6 signaling contributes to tumor cell proliferation, survival, epithelial–mesenchymal transition, and immune evasion. These oncogenic mechanisms highlight STAT6 not only as a driver of tumor biology but also as a potential prognostic biomarker and therapeutic target."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "23", "end_ref": "34"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nGenetic polymorphisms and variants within STAT6 have also been linked to allergic diseases and atopic phenotypes. Specific STAT6 single nucleotide polymorphisms modulate serum IgE levels and have been associated with an increased risk and greater severity of allergies such as nut hypersensitivity. These associations reinforce STAT6’s central role in mediating cytokine‑driven immune responses that underlie atopic disorders."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "35", "end_ref": "39"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nExternal factors further modulate STAT6 activity, thereby influencing its downstream signaling outcomes. For instance, pathogen‑derived kinases (as demonstrated with Toxoplasma gondii effectors) and platinum‑based chemotherapeutics can alter STAT6 phosphorylation dynamics, while vitamin D and other cytokine milieu components regulate its transcriptional potency. Such multifaceted regulation of STAT6 underscores its integral role in orchestrating both innate and adaptive immune responses as well as in shaping the tumor microenvironment."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "40", "end_ref": "43"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jie Yang, Saara Aittomäki, Marko Pesu, et al. 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