{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSNORD24 is a member of the box C/D small nucleolar RNAs that guides the 2′-O-methylation of ribosomal RNA, a modification critical for proper rRNA processing and ribosome biogenesis. Emerging evidence suggests that, beyond its canonical role in ribosome assembly, SNORD24 may influence cellular responses to tyrosine kinase inhibitors (TKIs) by modulating translational fidelity and protein synthesis. Such regulatory functions are of particular interest in the context of chronic myeloid leukemia (CML), where BCR-ABL-independent mechanisms contribute to TKI resistance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n \nDisruptions or alterations in SNORD24 expression could lead to aberrant rRNA modifications, thus subtly altering the ribosome’s structure and function. These changes may affect downstream cellular signaling pathways and stress responses, thereby providing leukemic cells with a survival advantage even in the presence of TKI therapy. This noncanonical activity of SNORD24 highlights its potential role in the complex molecular framework underpinning BCR-ABL-independent drug resistance in CML."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n \nIn summary, SNORD24’s established function in rRNA modification coupled with its emerging link to altered translational control may contribute to the development of TKI resistance in CML that is independent of BCR-ABL activity. Unraveling the mechanisms by which SNORD24 impacts ribosomal function and cellular adaptation holds promise for identifying novel therapeutic targets to overcome drug resistance."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Taewoo Yang, Kyu-Young Sim, Gwang-Hoon Ko, et al. "}, {"type": "b", "children": [{"type": "t", "text": "FAM167A is a key molecule to induce BCR-ABL-independent TKI resistance in CML via noncanonical NF-κB signaling activation."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Exp Clin Cancer Res (2022)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1186/s13046-022-02298-1"}], "href": "https://doi.org/10.1186/s13046-022-02298-1"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "35241148"}], "href": "https://pubmed.ncbi.nlm.nih.gov/35241148"}]}]}]}