ArticleCell death discovery2026
Identification and molecular typing of disulfidptosis-related biomarkers in anaplastic thyroid carcinoma.
Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
13 authors.
Funding
Abstract
Increasing evidence suggests that disulfidptosis plays a crucial role in tumorigenesis and progression. This study aimed to identify biomarkers closely associated with disulfidptosis in anaplastic thyroid carcinoma (ATC). Utilizing ATC-related datasets (GSE65144, GSE9115, GSE27155, and GSE53072) in conjunction with disulfide bond-related genes (DRGs) identified in the literature, differentially expressed genes (DEGs) were screened from the GSE65144 and GSE9115 datasets. A total of 113 common DEGs were identified through cross-sectional analysis. Weighted gene co-expression network analysis (WGCNA) was employed to screen genes related to disulfidptosis and ATC, and five biomarkers-ATP1B3, TFF3, LGALS1, ADAM12, and COL1A2-were identified using machine learning algorithms. A nomogram model constructed based on these markers demonstrated high accuracy. In vitro validation revealed that ATP1B3 knockdown significantly inhibited tumor growth, indicating its potential anti-ATC activity. Furthermore, laser confocal microscopy, flow cytometry, and other experimental methods suggested a correlation between ATP1B3 and disulfidptosis. These findings highlight ATP1B3, TFF3, LGALS1, ADAM12, and COL1A2 as potential disulfidptosis-related biomarkers in ATC. This study provides a theoretical foundation for understanding the role of disulfidptosis in ATC pathogenesis and suggests that ATP1B3 may serve as a promising therapeutic target.
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