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. 2024 Oct 25;22:281. doi: 10.1186/s12957-024-03568-2

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.

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Fig. 1 — The Role of TERT promoter hypomethylation in TC. A TERT promoter methylation levels in 56 normal thyroid tissues vs. 571 TC tissues; (B) TERT mRNA expression in TERT hypermethylated (n = 33) and hypomethylated (n = 530) TC samples; (C-F). Kaplan-Meier analysis reveals the association of TERT methylation with all PTC clinical outcomes, including overall survival (C), disease-specific survival (D), disease-free interval (E), and progression-free interval (F); (G-J). Kaplan-Meier analysis reveals the association of TERT methylation with clinical outcomes of advanced PTC (stage III/IV), including overall survival (G), disease-specific survival (H), disease-free interval (I), and progression-free interval (J). Reproduced under the terms of the CC-BY license [28]. Copyright © 2024 The Authors, published by Frontiers