{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nTCF12, a basic helix‐loop‐helix E protein also known as HEB, plays a vital role during embryogenesis and the development of multiple tissues. In the context of craniofacial and neurodevelopment, TCF12 functions by heterodimerizing with tissue‐specific transcription factors such as TWIST1 to synergistically regulate gene expression critical for normal suture formation; mutations or haploinsufficiency in TCF12 are strongly associated with craniosynostosis and have even been implicated in dyslexia and GnRH neuronal development. Moreover, alternative splicing within the TCF12 locus contributes to its complexity and tissue‐specific roles, while loss‐of‐function mutations give rise to distinct facial and auricular phenotypes that aid in clinical diagnosis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn several solid tumors, TCF12 exerts context‐dependent effects that regulate malignant progression. In colorectal, ovarian, cervical, lung, and esophageal squamous cell carcinomas—as well as in anaplastic oligodendroglioma, glioma, and prostate cancer—its deregulated expression impacts key cellular processes. In some cancers, overexpression of TCF12 promotes cell migration, invasion, epithelial–mesenchymal transition and metastasis (often via transcriptional repression of epithelial markers like E‐cadherin and through regulation by noncoding RNAs such as circRNAs and miRNAs), whereas in other settings, for example prostate cancer, TCF12 appears to restrain tumor aggressiveness. Thus, TCF12 emerges as a central node in transcriptional networks that either foster or inhibit oncogenic behaviors, depending on the cellular context."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "9", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the hematopoietic system and leukemogenesis, TCF12 participates in lineage specification and differentiation. It functions as a key transcriptional regulator during mesodermal and hematopoietic specification in embryonic stem cells and T cell development, and its activity is directly compromised by leukemogenic fusion proteins like AML1‐ETO. Furthermore, oncogenic rearrangements and alterations in the levels of TCF12—as well as its regulation by interacting partners (for example via a novel interaction with nuclear tubulin to modulate CXCR4 transcription)—underscore its significance in the control of normal hematopoiesis and in the pathogenesis of myeloid disorders."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "19", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "T-I Gan, L Rowen, R Nesbitt, et al. 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