{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nHMGA2 is a non‐histone, architectural transcription factor that modulates chromatin conformation to regulate multiple target genes involved in cell cycle control and differentiation. Several studies have demonstrated that HMGA2 is normally expressed during embryogenesis and is largely repressed in adult tissues by microRNAs such as the let‐7 family. In various tumors, however, genetic alterations – including chromosomal rearrangements that excise its 3′ untranslated region – and epigenetic dysregulation lead to aberrant HMGA2 overexpression. This loss of let‐7–mediated repression not only results in activation of oncogenic pathways (for example, via up‐regulation of cyclin A through interference with transcriptional repressors) but also enhances chemosensitivity in some contexts. Such findings highlight the dual nature of HMGA2 as a developmental regulator and as an oncogene when its normal silencing is disrupted."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn a wide array of cancer types – including lung, pancreatic, breast, melanoma, colon, ovarian, pituitary, and head and neck neoplasms – HMGA2 has been implicated as a key driver of epithelial–mesenchymal transition (EMT) and metastatic progression. Its overexpression promotes EMT by directly regulating critical transcription factors such as SNAIL, SLUG, and TWIST and by cooperating with TGF‑β/Smad and Wnt/β‑catenin signaling pathways. HMGA2 thereby enhances tumor invasiveness, metastatic dissemination, and resistance to therapeutic insults. Moreover, deregulated HMGA2 has been associated with aggressive tumor grades, poorer patient survival, and in many cases, serves as an independent prognostic marker across multiple studies."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "30"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its roles in tumor initiation and progression, HMGA2 has been linked to normal developmental processes such as determination of adult body stature and the balance between osteogenesis and adipogenesis. Genome‐wide association studies have implicated HMGA2 variants in human height, while deregulation of the let‐7/HMGA2 axis also influences mesenchymal stem cell differentiation. In addition, analyses of benign neoplasms – including uterine leiomyomas and salivary gland pleomorphic adenomas – have shown that HMGA2 overexpression or rearrangement can serve as a diagnostic marker and is mutually exclusive with other genetic alterations, underscoring its potential as a prognostic indicator and therapeutic target in both benign and malignant disease settings."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "31", "end_ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Michela A Tessari, Monica Gostissa, Sandro Altamura, et al. 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