{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMYB is a critical transcription factor in normal hematopoiesis and erythroid regulation. Several studies have demonstrated that sequence variants in the HBS1L‐MYB region modulate levels of fetal hemoglobin and red blood cell traits in hemoglobinopathies such as sickle cell disease and β‐thalassemia. In these contexts, reduced MYB activity is linked to the relief of γ‐globin repression, while MYB expression in hematopoietic progenitors is intricately regulated by microRNAs (for example, miR-15a and miR-150) that establish autoregulatory feedback loops essential for lineage commitment and proper differentiation of CD34⁺ cells – processes that also affect the function of inflammatory cells such as eosinophils."}, {"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 a variety of malignancies, aberrant activation of MYB through diverse mechanisms—including gene fusions, tandem duplications, and super‐enhancer translocations—has emerged as a pivotal driver of oncogenesis. Recurrent rearrangements such as MYB–NFIB fusions observed in adenoid cystic carcinomas, T-cell receptor–mediated translocations and copy number duplications in T-cell acute lymphoblastic leukemia, as well as MYB–QKI fusions in low-grade neuroepithelial tumors, underscore how MYB dysregulation can lead to uncontrolled proliferation, impaired differentiation, and ultimately tumor development."}, {"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": "\nMYB also contributes significantly to the biology of various solid tumors. In breast and prostate cancers, for example, MYB functions as an effector of steroid hormone signaling while its overexpression is driven by estrogen or androgen deprivation. Similarly, in non–small cell lung cancer, microRNAs such as miR-195 suppress MYB, highlighting its role as a mediator of tumor cell proliferation and survival. In B-cell chronic lymphocytic leukemia, MYB can stimulate the transcription of oncogenic microRNA clusters, further emphasizing its broad impact on tumorigenesis across different tissue types."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "23", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, MYB operates as a central transcriptional regulator that governs cell cycle progression through its cooperation with multiple co-factors and regulatory complexes. It helps recruit and coordinate complexes such as the DREAM complex and the MuvB-FOXM1 module to activate late cell cycle genes like cyclin B1, and its interactions with specific RNA-binding proteins further influence the maintenance and function of leukemia stem cells. These multifaceted activities not only underscore MYB’s role in controlling proliferation but also position it as a potential target for therapeutic intervention."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jie Jiang, Steve Best, Stephan Menzel, et al. 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